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1
Suliman, Khanfer Riyad. "Psychological stress and neutrophil function." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3093/.
Повний текст джерелаАнотація:
Little is known about neutrophil function, an important component of innate immunity, in relation to psychosocial factors. This thesis investigated the effect of acute and chronic psychological stressors on human neutrophil function among young and older adults. The first two studies examined the effects of an acute laboratory psychological stress task on neutrophil function in young and older adults, respectively. Blood samples to determine neutrophil function were taken at resting baseline, during acute stress and during recovery. In the first study (N=40), there was an acute increase in phagocytic ability and a reduction of superoxide production associated with the stress task relative to baseline. In study two (N =17), there was a significant reduction of neutrophil superoxide production associated with the stress task. Study three (N=48) examined the effect of chronic stress, a recent bereavement (<2 months), on neutrophil function in elders. Cortisol and dehydroepiandrosterone-sulphate (DHEAS) levels were determined in serum to assess potential mechanisms. Superoxide production was significantly reduced among the bereaved group when challenged with E. Coli; also, the bereaved had a significantly higher cortisol:DHEAS ratio compared to controls. Overall, this thesis shows that human neutrophil function is sensitive to both acute and chronic psychological stress exposures; however, more research is needed to determine the specific underlying mechanisms behind the observed alterations.
2
Ade, Carl Jacob. "Cardiorespiratory and vascular function during stress." Diss., Kansas State University, 2013. http://hdl.handle.net/2097/15976.
Повний текст джерелаАнотація:
Doctor of PhilosophyDepartment of Anatomy and Physiology
Thomas J. Barstow
The primary aim of this dissertation was to evaluate the factors that contribute to the cardiorespiratory and vascular responses following exercise conditioning and microgravity deconditioning. The first study of this dissertation (Chapter 2) revealed that exercise training in the head down tilt posture, which places increases central blood volume compared to upright, results in cardiorespiratory adaptations in both upright and head down tilt postures which are not completely expressed with exercise training in the upright posture. These findings suggest that augmentation of the ventricular volume load during exercise training may result in adaptations that transfer across multiple body positions. In the second and third studies measurements of blood velocity and flow were performed via Doppler ultrasound. In Chapter 3 we observed that in the brachial and femoral arteries blood moves with a slightly blunted parabolic velocity profile that is very stable across a range of mean arterial pressures and downstream limb resistances. We concluded that these findings support the current calculations of shear rate based on the assumptions of laminar flow. With these assumptions confirmed, the investigation in Chapter 4 could be performed. We observed that acute exposure to a sustained antegrade shear rate, via unilateral forearm heating, increased measurements of flow-mediated dilation and the overall rate of adjustment for forearm blood flow and vascular conductance during dynamic handgrip exercise. These findings suggest that one potential stimulus for improvements in vascular function and health following exercise conditioning may be exposure to elevations in antegrade shear. Lastly in Chapter 5 we changed focus to the cardiorespiratory deconditioning following long-duration microgravity exposure. We retrospectively reviewed and analyzed previous investigations of microgravity deconditioning and demonstrated that the decrease in maximal O2 consumption ( O2max) occurs as a function of duration of exposure and that both convective and diffusive O2 transport pathways substantially contribute to this decline. In addition we reviewed the current literature and highlighted potential mechanisms, across several organ systems, which may contribute to this decline in O2max. Collectively, these studies revealed the breath of plasticity for cardiorespiratory adaptations to a variety of stressors.
3
Anderson, Richard Anthony. "Lipids, oxidative stress and endothelial function." Thesis, King's College London (University of London), 2004. https://kclpure.kcl.ac.uk/portal/en/theses/lipids-oxidative-stress-and-endothelial-function(ca261d48-d716-4156-9a38-dbb72775b36a).html.
Повний текст джерела
4
Ikeme, Patience Obianuju. "Human ecological stress and menstrual function." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360734.
Повний текст джерела
5
Zhao, Youhao. "Stress-Function Variational Method for Stress Analysis of Adhesively Bonded Joints." Thesis, North Dakota State University, 2014. https://hdl.handle.net/10365/27271.
Повний текст джерелаАнотація:
Recently, adhesively bonded joints (ABJs) has found more rapidly increasing applications in aerospace and aeronautical structures, ground vehicles, and flexible electronics than mechanical fastening and welding technologies. However, outstanding issues still exist. This work was to develop a systematic semi-analytic method for accurate prediction of the interfacial shear and normal stresses of ABJs. Two unknown shear and peeling stress functions at each interface was first introduced in formulation, which satisfies all the traction boundary conditions. A set of governing ordinary differential equations (ODEs) was determined via triggering the theorem of minimum complimentary strain energy. Matlab? code was programmed to execute the proposed method. Furthermore, the present method was validated by finite element method and compared with those models in the literature. The present method is applicable for convenient scaling analysis and optimal design of ABJs and other types of ABJs such as adhesively bonded tubular and composite joints, etc.NSF; ND NASA EPSCoR; Faculty Research Initiative Grant; Department of Mechanical Engineering at NDSU.
6
Jadavji, Nafisa M., and University of Lethbridge Faculty of Arts and Science. "Interactions of stress and motor system function." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/662.
Повний текст джерелаАнотація:
Stress is one of the most critical influences on behavior, performance and disease.
Recent findings from our laboratory have shown that stress represents a major
modulator of motor function in the intact and damaged brain. The mechanisms by
which stress and stress hormones affect motor system function, however, have not yet
been determined. The objective of this thesis was to determine the route of action of
stress and stress hormones on the motor system in a rat model. The first experiment
investigates whether corticosterone is involved in mediating stress-induced motor
impairments. The second experiment compares the role of glucocorticoid and
mineralocorticoid receptors in regard to modulating the motor response to stress. The
third experiment determines the differential effects of stress on motor function in
males and females. The final experiment systematically describes changes in neuronal
cell signaling that affect normal function of motor areas. The results indicate that
disturbance of fine motor control by stress is not associated with stress hormone
increases. Furthermore, it is modulated through the glucocorticoid and
mineralocorticoid receptors. Stress differentially impairs motor function in males and
females. These changes in motor behaviour could possibly be the result of changes in
neuronal cell signaling within the motor system. This research provides new insights
into physiological influences in motor system function and disorders of the motor
system.ix, 128 leaves : ill. (some col.) ; 29 cm.
7
McCulloch, Andrew C. "The stress radionuclide assessment of diastolic function." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1878/.
Повний текст джерелаАнотація:
Background Many patients are referred from primary care with suspected heart failure and are found to have preserved systolic function. These patients may be labelled as having normal ejection fraction or diastolic heart failure, the diagnosis of which is both controversial and difficult. Previous work has identified a large proportion of these patients to have an alternative, pre- existing diagnosis. This thesis prospectively assesses the prevalence of undiagnosed ischaemic heart disease and respiratory disease in this patient group and assess diastolic function using multiple methods. The central hypothesis being tested was that first third fractional filling, a radionuclide ventriculogram (RNVG) parameter previously used to assess diastolic function at rest, would identify diastolic dysfunction more accurately under stress conditions. Methods Patients were recruited from an open access echocardiography service. Echocardiography, including tissue Doppler assessment, was carried out independently by 2 experienced observers. Confounding diagnoses including coronary artery disease and respiratory disease were actively sought by myocardial perfusion imaging and spirometry. N-terminal proBNP was measured. List mode radionuclide ventriculography was performed at rest supine and during upright bicycle exercise with simultaneous measurement of VO2 max. Validation of the reliability and reproducibility of first third fractional filling, peak filling rate, time to peak filling and other radionuclide parameters of systolic and diastolic function was undertaken. This demonstrated that it was possible to measure both first third fractional filling and peak filling rate with the short acquisition times necessary for assessment during stress. Time to peak filling was poorly reproducible under these conditions. A normal range for first third fractional filling at rest and during exercise was established. Due to a strong inverse relationship between heart rate and first third fractional filling, a continuous reference range was constructed using an exponential model. This unique approach enables the calculation of the lower limit of normal at any heart rate. A more conventional mean ± 2 standard deviations was used for the other RNVG parameters. Results Eighty three patients were recruited and completed an extensive multi-modality assessment of systolic and diastolic function. As with previous work in this field, the patients were predominantly female (82%) and elderly (mean age 66.7). Mild left ventricular systolic dysfunction as determined by RNVG was missed by echocardiography in one third of patients. Systolic dysfunction more significant than this was not observed. N-terminal proBNP was elevated in 21 of 82 patients where it was available with no significant difference in left ventricular ejection fraction between those with normal and elevated levels. Myocardial perfusion scanning was normal in 46 of 83 patients and showed significant ischaemia in 20 of 83. Spirometry was normal in 58 of 82 patients, with mild airflow obstruction in 20 patients and moderate obstruction in 4. In only one patient were no alternative diagnoses present. There was poor correlation between indices of diastolic function at rest including first third fractional filling, echocardiographic parameters and NT-proBNP. The assessment of diastolic function using stress radionuclide ventriculography did not improve the correlation between measured indices. On stress, however, low first third fractional filling predicted exercise intolerance as an inability to reach anaerobic threshold. Conclusions Alternative diagnoses to diastolic dysfunction are present almost universally in patients with suspected normal ejection fraction heart failure. This is true even where these diagnoses are not previously established. This thesis underlines the need to fully assess this patient group to allow appropriate targeting of therapy. It is also clear that echocardiography alone is potentially misleading and it is suggested that it is better placed within a tiered assessment process. The assessment of diastolic function using stress radionuclide ventriculography, although an appealing concept, does not improve diagnostic accuracy within this patient group. The marked heterogeneity of this patient group is likely to have played a role in this and it may be of interest to reassess stress radionuclide ventriculography in a more acute heart failure population.
8
Isaac, Claire L. "Cognitive function in post-traumatic stress disorder." Thesis, University of Warwick, 2002. http://wrap.warwick.ac.uk/2358/.
Повний текст джерелаАнотація:
Complaints of poor memory by individuals with posttraumatic stress disorder (PTSD) have engendered research into attention and memory functioning in this disorder. Due to numerous methodological difficulties encountered in research with this group, results have been inconclusive. In Chapter 1 of this thesis the existing literature is reviewed to ascertain whether there is any evidence of a specific pattern of memory disorder associated with PTSD. Studies are reviewed for evidence of cognitive deficits relating to the structures of the limbic system. dysfunction in which has been implicated in PTSD. It is concluded that there is relatively good evidence of deficits related to probable frontal lobe functions. However, there is very little evidence of hippocampal related disorders and no studies have investigated memory functions relating to hypothesised roles of the amygdala in this group. In chapters 2 and 3 experiments are described that aim to investigate cognitive abilities related to amygdala functioning in PTSD. Chapter 2 investigates an hypothesised role of the amygdala in the consolidation of memory for emotional material. The results confirm the possibility of amygdala dysfunction in PTSD by showing that on a test of free recall participants with PTSD forgot emotional word stimuli at a faster rate than control participants, whereas non-emotional stimuli were forgotten at a more normal rate. Chapter 3 investigated a second hypothesised role for the amygdala in the recognition of facial expressions of fear and anger. Results showed that PTSD participants were somewhat impaired in their recognition of these expressions, which contrasted with an enhanced ability, associated with symptoms of hyperarousal, in identifying other negative facial expressions. In Chapter 4, the relevance of neuropsychological research to Clinical Psychology is discussed. It is argued that such research is vital if we are to fully understand the difficulties clients could face on a day-to-day basis.
9
Lu, Dan. "ATF3, a stress-inducible gene function and regulation /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1155740569.
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10
Poirier, Patrick. "Effect of chronic stress on prefrontal cortical function." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86861.
Повний текст джерелаАнотація:
The prefrontal cortex (PFC) is a brain region thought to mediate cognitive functions such as working memory. Chronic stress has been shown to reduce working memory. In this thesis study, the effect of chronic stress on PFC functions was assessed in adult rats.First, contrary to previous evidences, chronic stress induces working memory performance alterations differentially in two populations of rats. One group displayed a decrease of performance only at 30 second delay, while the other had a decrease and increase at 0 and 30 seconds respectively.
Then, the effect of chronic stress on synaptic plasticity induction in the hippocampus-PFC network was investigated. High-frequency tetanic stimulation (HFS) of the dorsal hippocampus that induced long-term potentiation (LTP) in the prelimbic and infralimbic cortex in normal conditions was unable to induce LTP after chronic stress in the infralimbic cortex, whereas long-term depression (LTD) instead of LTP was induced in the prelimbic cortex.
Given that synaptic plasticity has been shown to depend on NMDA receptors in the PFC, NMDA subunit expressions before and after chronic stress was examined. There was a decrease of NR1 subunits expression in the prelimbic, but not infralimbic cortex. In contrast, the NR2A/NR2B ratio was increased in the infralimbic, but not prelimbic cortex. These results suggest that chronic stress disrupts PFC functions through dynamic modulation of distinct neural networks within the PFC.
Le cortex préfrontal (PFC) est une région du cerveau qui contrôle les fonctions cognitives comme la mémoire de travail. Dans cette thèse, l'effet du stress chronique sur des fonctions du PFC a été analysé chez des rats adultes.
Premièrement, les performances de la mémoire de travail ont été mesurées avant et après exposition au stress chronique. Nous avons constaté que le stress chronique induit des changements de performances de la mémoire de travail différemment selon deux populations de rats. Une des populations a démontré une diminution de performance seulement à 30 secondes de délai. Au contraire, l'autre a démontré une diminution de performance à 0 seconde et une amélioration de performance à 30 secondes.
En plus, nous avons évalué l'effet du stress chronique sur l'induction de la plasticité synaptique dans le réseau reliant l'hippocampe au PFC. Dans les conditions initiales, une stimulation tétanique à haute fréquence (HFS) dans l'hippocampe dorsal provoquait une potentialisation à long terme (LTP) dans le cortex prélimbique et infralimbique Or après exposition au stress chronique, une stimulation tétanique à haute fréquence n'a pas entraîné de potentialisation à long terme dans le cortex infralimbique. De plus, une exposition au stress chronique a provoqué l'apparition dans le cortex prélimbique d'une dépression à long terme (LTD) plutôt qu'une potentialisation à long terme.
Étant donné que la plasticité synaptique dépend des récepteurs de NMDA dans le PFC, nous avons examiné l'expression de sous-unité de NMDA avant et après exposition au stress chronique. En accord avec les changements synaptiques distincts de plasticité entre le cortex prélimbique et infralimbique après exposition au stress chronique, nous avons observé que l'expression de la sous-unité NR1 a diminué dans le prélimbique, mais non dans l'infralimbique. En revanche, le ratio de NR2A/NR2B a augmenté dans le cortex infralimbique, mais non dans le prélimbique. Ces résultats suggèrent que le stress chronique perturbe les fonctions du PFC par la modulation dynamique des réseaux distincts neurologiques dans le PFC.
11
Vitlić, Ana. "Chronic stress and ageing : effects on immune function." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5365/.
Повний текст джерелаАнотація:
The research in this thesis is concerned with the effect of chronic stress, caregiving and bereavement, and ageing on immune and endocrine parameters. First, there was no difference in serum anti-CMV antibody titre between younger caregivers and matched controls, but CMV seropositive caregivers with more negative health behaviours had higher CMV antibody titre. Second, there was no difference in neutrophil function between caregivers and controls in both younger and older group, while only younger caregivers showed a higher serum cortisol:cortisone ratio than controls. Further, those caregivers that reported higher anxiety and burden symptoms had lower neutrophil phagocytosis. Third, caregivers had more senescent KLRG1\(^+\) T cells than controls, but comparable number of “exhausted” PD-1\(^+\) T cells and thymic output. Finally, young bereaved adults showed similar neutrophil function and serum cortisol and DHEAS levels as non-bereaved controls, whereas older bereaved adults had impaired neutrophil function and a higher cortisol:DHEAS ratio. These findings suggest that chronic stress can have differential effects on immune and endocrine parameters, but in some cases, presence of immunosenescence is required for immune decrements to be observed. Further, they emphasise the importance of focusing on the individual's response to chronic stress rather than their chronic stress status, per se.
12
Carragher, J. F. "The effects of stress on reproduction function in trout." Thesis, Brunel University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383742.
Повний текст джерела
13
Sitar, Sandra M. "Effects of oxidative stress and propofol on astrocyte function." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ39884.pdf.
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14
Jones, Philip Hugh. "The impact of stress on visual function in nystagmus." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/15155/.
Повний текст джерелаАнотація:
Infantile Nystagmus Syndrome (INS) is defined as a constant involuntary movement of the eyes, affecting 0.12% of the population. Previous research shows that eye movements in patients with nystagmus increase in stressful conditions, and they report that their vision gets worse. However, there have been no definitive conclusions as to the effect of stress on visual acuity (VA). The aim of the studies described here was to assess visual function, including VA, during periods of stress. The results showed that there was no difference in VA measured with horizontally and vertically oriented Landolt C’s, but, in agreement with published research, VA was found to be poorer when using vertically oriented gratings as compared to horizontal gratings. Using a Trans-Cutaneous Electrical Nerve Stimulation (TENS) machine, an effective clinical stressor, we confirmed that the intensity of nystagmus increased when under stress; however VA, as measured using Landolt Cs, was not affected. Patient response time also increased during stressful periods and was significantly longer in INS than in control subjects. Using a questionnaire, we identified the most stressful situations for patients with nystagmus as being: “finding a person in a crowd” and “crossing a road in heavy traffic”. Under stress, rather than vision becoming blurred, patients with nystagmus reported that they “take longer to see things” and “have difficulty with seeing facial features and small detail”. The results reported here have important implications for patients with nystagmus in the real world, strongly suggesting that, although maximum acuity is unaffected by stress, more time should be allowed for tasks at both work and school. Further research is required to fully understand the changes in other aspects of visual function with stress.
15
Stevanin, Tania Maria. "Bacterial flavohaemoglobins : physiological function and responses to nitrosative stress." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340137.
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16
Gheorghe, Delia. "Investigating the effects of psychosocial stress on cerebellar function." Thesis, University of East Anglia, 2018. https://ueaeprints.uea.ac.uk/70267/.
Повний текст джерелаАнотація:
Differences in cerebellar structure and function are consistently reported in individuals exposed to early-life stress and individuals with diagnosed stress-related psychopathology. Despite this, current neurobiological models of stress have not considered the role of the cerebellum in the regulation of the stress response. Furthermore, it is unclear the mechanism by which stress may affect cerebellar function. The studies presented in this thesis set out to address these questions by exploring the relationship between acute psychosocial stress and the cerebellum. To achieve this, two putative cerebellar functions were investigated: saccadic adaptation and postural balance control. Chapters 4 and 5 present two studies, which evaluated the effectiveness of each task, as well as individual differences in task performance. Chapter 4 presents evidence demonstrating a linear effect of saccadic adaptation across participants. Chapter 5 revealed improved postural balance control under perturbed balancing conditions. Individual differences in task performance were inconclusive. Each study was followed by an investigation on the effects of acute psychosocial stress on task performance. Particularly, Chapter 6 demonstrated that stress impaired the rate of saccadic adaptation, and that this impairment was associated with the stress-related endocrine response. The study presented in Chapter 7 showed no effect of psychosocial stress on postural balance control. Finally, Chapter 8 explored the effects of non-invasive cerebellar stimulation on saccadic adaptation and cortisol output, revealing that a decrease in cerebellar excitability yielded adaptation rates that were similar to those observed after stress. These findings suggest that psychosocial stress impairs error-driven feedforward computations specifically, via glucocorticoid signalling, thus contributing to the current neurobiological models of stress.
17
Walter, Kristen H. "Self-control and executive function in posttraumatic stress disorder." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1276474763.
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18
Movsisyan, Tatevik. "Perceived Stress and Visual Function in Macular Degeneration Patients." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1461087205.
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19
Basoalto, Hector Christian. "Weight function formalism applied to crack bridging problems." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243985.
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20
Wang, Xiao. "Stress-Function Variational Methods for Stress Analysis of Composite Laminates and Adhesively Bonded Composite Joints." Thesis, North Dakota State University, 2015. https://hdl.handle.net/10365/27639.
Повний текст джерелаАнотація:
Adhesively bonded composite joints (ABCJs) have been broadly used to connect multimaterials
and show their structural and economic advantages compared to traditional bonding
methods. However, robust methods are still desired for efficient and accurate lay-wise stress
analysis of ABCJs involving multiple boundaries and layers.
The purpose of this work was to extend the stress-function variational method for free-edge
stress analysis of composite laminates with a finite length. At each interface of the laminate, two
unknown Lehknitskii?s stress potential functions were introduced to interpolate the stresses
across the layer. A set of 4th-order governing ODEs of the functions was obtained via evoking the
complementary virtual work, solved by eigenvalue-function method under proper traction
conditions. Corresponding MATLAB? program was developed and validated by the FEM
(ANSYS?). This method can also examine the stress-suppression effect after composite
laminates interleafing. Consequently, the above method was furthered for determining the laywise
stress distribution in ABCJs.
21
Genot, Baptiste. "Functional characterization of the stress-activated Arabidopsis MAP Kinase MPK3 using gain-of-function mutations." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLE010.
Повний текст джерелаАнотація:
Les plantes détectent les pathogènes dans leur environnement et s’y adaptent pour survivre. Le groupe Stress Signalling de l’IPS2 cherche à décrire les mécanismes cellulaires mis alors en jeu et à proposer des stratégies permettant de développer des cultures plus résistantes aux stress. Les modules Mitogen-Activated Protein Kinases (MAPKs) semblent être des acteurs clés de la transduction du signal: ils sont en effet très rapidement activés par de nombreux stress et notamment par les Pathogen-Associated Molecular Patterns (PAMPs). Des approches de génétique, utilisant des mutants perte-de-fonction, ont montré que ces modules MAPKs régulaient de nombreux aspects de l’adaptation des plantes à leur environnement.Dans notre laboratoire, nous avons précédemment identifié des mutations capables de rendre les MAPKs de la plante modèle Arabidopsis thaliana constitutivement actives (CA). L’objectif de mon projet était de clarifier les rôles spécifiques des MAPKs activées par le PAMP flg22 à l’aide de ce nouvel outil. Pour cela, j’ai créé des plantes exprimant des CA MAPKs et j’ai caractérisé leur phénotype en conditions normales de croissance ou lors d’interactions avec des pathogènes. Je me suis particulièrement intéressé à la MAPK MPK3. J’ai montré que des plantes exprimant une version CA de MPK3 avaient un phénotype d’auto-immunité caractérisé par un nanisme associé à la mort cellulaire spontanée et à une accumulation de formes activées de l’oxygène. Des études métabolomiques, transcriptomiques et de génétique ont permis de préciser les réponses régulées par cette MAPK. J’ai en particulier montré que le phénotype des plantes CA-MPK3 était dépendant de la protéine EDS1 (Enhanced Disease Susceptibility 1), un régulateur primordial des réponses aux pathogènes, et partiellement dépendant de l’acide salicylique. J’ai également créé et caractérisé des plantes exprimant des formes CA de MPK6 et MPK11.En conclusion, mon travail tirant partie des mutations CA a permis de proposer de nouveaux rôles spécifiques pour certaines MAPKs activées par le stress. Mes résultats préliminaires suggèrent également que les plantes exprimant des CA MAPK peuvent présenter une meilleure résistance aux pathogènesPlants can detect pathogens in their environment and adapt to survive it. The Stress Signalling group in IPS2 aims to decipher cellular mechanisms occurring after pathogens detection and to propose strategies to develop stress-resistant crops. Mitogen-Activated Protein Kinases (MAPKs) modules define key actors of signal transduction. MAPKs are indeed quickly activated in response to various stresses including pathogens-associated molecular patterns (PAMPs). Genetic approaches using loss-of-function mutants showed that MAPK modules regulate many aspects of plant adaptation to their environment.In our laboratory, we previously identified mutations which render MAPKs constitutively active (CA) in the plant model Arabidopsis thaliana.The main objective of my thesis was to clarify the specific roles of MAPKs activated by the PAMP flg22 using this new tool. For this, I created plants expressing CA MAPKs and characterized them in normal growth conditions or after pathogen infections. I mainly focused my project on the MAPK MPK3. I showed that plants expressing a CA version of MPK3 had an auto-immune phenotype characterized by a severe dwarfism, spontaneous cell death and accumulation of reactive oxygen species. Transcriptomic, metabolomic and genetic studies were performed to understand which pathways are regulated by this MAPK. This work demonstrates that MPK3 is a positive regulator of plant immunity, whose function depends on EDS1 (Enhanced Disease Susceptibility 1), a key regulator of pathogens responses, and partially depends on the phytohormone salicylic acid. I also created and characterized plants expressing constitutively active MPK6 and MPK11. In conclusion, CA mutations allowed us to reveal new specific roles for several stress-activated MAPKs. My preliminary results also suggest that plants expressing CA MAPK may have a better resistance to pathogens
22
Wolfgang, Curt Douglas. "A study of the biological function of ATF3 : stress inducibility, target promoters and functional consequences /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu148819244742789.
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Berger, Christine Elizabeth Marie. "Superoxide anion in osteoclast and osteoblast function." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265210.
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24
Andrews, Leanne. "The structure and function of trauma-related avoidance." Thesis, University of Essex, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248634.
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25
Campbell, Ross I. "Arterial function, physiological stress and the role of nitric oxide." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/55170/.
Повний текст джерелаАнотація:
Cardiovascular disease is the leading cause of death in the western world. Hypertension is a major risk factor for cardiovascular diseases and blood pressure is in turn markedly influenced by large artery stiffness. Recently a number of studies have reported that apparently healthy normotensive individuals who exhibit an exaggerated systolic blood pressure response on exercise are at increased risk of developing subsequent sustained hypertension and cardiovascular disease. It is likely that an exaggerated systolic blood pressure response on exercise represents an abnormal response of the large artery during dynamic exercise. In this thesis the normal responses of large arteries to different types and intensities of exercise was investigated in healthy normotensive subjects. Whilst distensibility of limb conduit arteries was measured for up to 15 minutes following exercise aortic distensibility did not change. An exaggerated systolic blood pressure response on exercise was not observed in healthy subjects without other conventional cardiovascular risk factors, but was observed frequently in the presence of such risk factors. Subjects with an exaggerated systolic blood pressure response on exercise did not show increased limb conduit artery distensibility immediately following exercise (and by implication during exercise). Blockade of NO synthesis prevented the increase in limb conduit artery distensibility seen in the first few minutes following exercise, but did not abrogate the more sustained increase in arterial distensibility following exercise. Systemic blockade of NO synthesis caused marked changes in systemic haemodynamics at risk, but these were markedly attenuated during exercise. The impact of mental stress on arterial function was also assessed. Whilst peripheral microvessels vasodilated, large arteries stiffened and this largely accounted for the observed increase in blood pressure.
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Fogl, Claudia Liliane Fiona. "Structure and function of the cardiac stress response protein MS1." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9408.
Повний текст джерелаАнотація:
Myocyte Stress 1 (ms1)/Striated muscle Activator of Rho Signalling (STARS), also known as Actin Binding Rho Activator (ABRA), is a 375 amino acid protein. Its expression increases one hour after the induction of stress in rat hearts through aortic banding. This expression precedes that of early response genes such as c-fos and c-jun. This process has been implicated in the development of left ventricular hypertrophy. ms1/STARS binds to actin, and deletion mutations had shown that residues 234-375 were necessary for actin binding. A mixture of combinatorial domain hunting and rational domain design gave a series of possible domains. Circular dichroism and nuclear magnetic resonance spectroscopy were used to characterise these domains. The first three domains, MSD1 (residues 2-118), MSD2 (40-196) and actin binding domain 1 (ABD1, 193-296) were unfolded, while ABD2 (294-375) was folded. Actin co-sedimentation assays showed that only ABD1 and ABD2 bound to actin. They bound to actin independently. The structure of ABD2 was determined using NMR. Mutation studies, based on the NMR structure and on data about the conservation of positively-charged regions in ms1/STARS homologues, were used to identify the actin binding surface of ABD2. The structure of ABD2 was shown to be a winged helix-turn-helix domain. These domains are often DNA binding domains. When DNA binding was attempted, it was shown that ABD1, ABD2 and the tandem of ABD1 and ABD2 bound to DNA. The identification of the actin binding domain and the discovery of a novel DNA binding ability open up many more possible functions of ms1/STARS.
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McGleenon, Bronagh Mary. "Endothelial function and measures of oxidative stress in Alzheimer's disease." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301745.
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Holt, Stephen Geoffrey. "Oxidant stress as a regulator of renal function in disease." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324675.
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Nelligan, Julie. "Anxiety and autonomic nervous system function during stress and recovery." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1060797984.
Повний текст джерелаАнотація:
Thesis (Ph. D.)--Ohio State University, 2003.Title from first page of PDF file. Document formatted into pages; contains xiii, 127 p.; also includes graphics Includes bibliographical references (p. 91-105). Available online via OhioLINK's ETD Center
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Potter, Claire. "Role of chronic shear stress in endothelial form and function." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11106.
Повний текст джерелаАнотація:
Endothelial cells in vivo exist in a dynamic environment, subject to the physical forces of blood flow as it is regulated through the cardiac cycle. Arguably, the most important force endothelial cells are subject to is shear stress, the frictional force of blood flow across the cell surface. Areas of the vasculature that experience laminar shear stress appear resistant to the development of atherosclerotic plaques, whereas those that experience low shear stress, due to complex patterns of blood flow, appear susceptible. In vitro study of the effects of chronic shear stress on the endothelium has been somewhat limited, due to the methods of modelling shear stress available, which are for the most part only suitable for culture for up to 24 hours. I have validated an orbital shaker method of modelling two flow environments seen in the vasculature, unidirectional flow and non-directional flow, with associated shear stress profiles, for chronic time periods of up to 7 days. I have shown clear differences between the two environments in terms of endothelial cell morphology and protein expression and identified many ways in which sheared cells differ from their static counterparts, in terms of morphology, protein expression, vascular mediator release and transcriptional profile. Shear stress appears to be a protective force, inhibiting expression of inflammatory mediators and significantly altering response to inflammatory stimulus. The orbital shaker may prove a useful model for in vitro study of the endothelium in a situation similar to that of physiological conditions.
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Singh, Nivedita. "Vascular relaxant function and oxidant stress in healthy older subjects." Thesis, St George's, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398220.
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Wiczynski, Teresa. "Interactions between Aerobic Exercise Volume, Academic Stress, and Immune Function." TopSCHOLAR®, 2018. https://digitalcommons.wku.edu/theses/2334.
Повний текст джерелаАнотація:
Many college students exercise individually or participate in collegiate and intramural sports in addition to fulfilling their stressful academic requirements. The combination of accumulated stress and vigorous exercise could result in an impaired immune system, prompting the onset of disease and absences in class and sports practice.
Twenty-six male and female participants aged 18 to 23 were recruited for this study. Over the course of an academic semester, participants completed weekly electronic surveys documenting stress levels, aerobic exercise, and symptoms related to upper respiratory tract infections. Participants were evaluated at four different time points (Baseline, Post-Midterm Exam, Baseline Reassessment, and Post-Final Exam) for body fat percentage, cardiovascular fitness, heart rate, blood pressure, and a 10mL blood draw. Blood samples were used to measure blood glucose, cortisol, IL-6, and CD11b levels. Analysis of cortisol and IL-6 concentrations required ELISA kits for protein quantification in plasma samples. CD11b levels in peripheral blood mononuclear cell samples were measured by Western Blot analysis.
There was a significant increase in blood pressure during the final exam compared to rest for systolic (p=0.005) and diastolic (p=0.004) blood pressures. There was a significant decrease in anxiety during the final exam compared to anxiety during the mid-term exam (p=0.022). The acute stress of an exam was strong enough to illicit physiologic blood pressure change, but the chronic stress throughout the semester was not intense enough did not illicit physiologic or immune responses. The volume of aerobic exercise in the vigorous workout group was not great enough to influence immune responses nor disease incidence.
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Tomeo, Nicholas Anthony. "Correlates between Chronic Stress and Executive Function in College Students." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1416233242.
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Cavaco, Fernando Almeida. "Human relations on board merchant ships : a function of leadership." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261272.
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Gomes, Mariana Lourenço Mocho Fernandes. "Lifestyle impact on human sperm function." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/14848.
Повний текст джерелаАнотація:
Mestrado em Biologia Molecular e CelularOxidative stress (OS) is believed to be an important cause of male infertility, which accounts for about half of all infertility cases. Reactive species (RS)- induced OS is detrimental to spermatozoa, leading to the damage of many biomolecules, such as lipids, proteins and DNA. Several lifestyle factors, such as alcohol and tobacco consumption, are known to induce OS and have been studied for their negative effects on male reproductive system. The aim of this study was to evaluate the impact of acute lifestyle changes, namely alcohol and tobacco consumption, on semen quality, accessory glands function and oxidative balance of sperm cells. Furthermore, the correlation between the OS parameters analyzed and the basic semen parameters was also assessed. Male students, in reproductive age, who participated in the academic festivities, donated a semen sample at three time points: before and one week and three months after the academic festivities. Basic semen analysis was performed and, subsequently, semen samples were processed. Acessory glands function was evaluated and OS was analyzed through measurement of the total antioxidant capacity of the sperm cells and through determination of the expression of antioxidant enzymes glutathione peroxidase 4 and superoxide dismutase 1. The impact of ROS in spermatozoa was also assessed through the determination of the protein carbonyl and 3-nitrotyrosine groups. The results indicate that a decrease in semen quality, demonstrated by a decrease in progressive motility and neutral α-glucosidase concentration and an increase in tail defects, occurs due to lifestyle alterations. The total antioxidant status of sperm cells and variations in protein oxidation levels are dependent on the alcohol and tobacco consumption. Moreover, some correlations were observed between the studied parameters, which may be useful in a clinical perspective. In conclusion, the lifestyle alterations are responsible for a decrease in semen quality and by an increase in protein modifications, which may consequently lead to a decrease in fertilizing potential.
O stress oxidativo (OS) tem sido considerado uma causa importante da infertilidade masculina, que está envolvida em cerca de metade dos casos de infertilidade. O OS induzido pelas espécies reativas (RS) é prejudicial para os espermatozoides, levando a lesões em várias biomoléculas, como os lípidos, proteínas e DNA. Alterações no estilo de vida, como o consumo excessivo de álcool e tabaco, induzem o OS e têm sido extensivamente estudadas devido aos seus efeitos negativos ao nível do sistema reprodutor masculino. O objetivo deste estudo foi analisar o impacto de alterações agudas no estilo de vida, nomeadamente o consumo de álcool e tabaco, na qualidade seminal, na função das glândulas acessórias e no equilibrio oxidativo dos espermatozoides. Para além disso, outro objetivo deste trabalho foi avaliar a possível relação entre os parâmetros de OS e os parâmetros seminais analisados. Estudantes masculinos, em idade fértil, que participaram nas festividades académicas, doaram uma amostra de sémen em três períodos de tempo: antes e uma semana e três meses após as festividades académicas. A análise básica ao sémen foi realizada e, posteriormente, as amostras foram processadas. A função das glândulas acessórias foi avaliada, assim como determinada a capacidade antioxidante total das células, a expressão das enzimas antioxidantes superóxido dismutase 1 e glutationa peroxidase 4 e a presença de grupos carbonilo e 3-nitrotirosina. Os resultados indicam que uma diminuição na qualidade seminal, demostrada por um decréscimo na motilidade progressiva dos espermatozoides e na concentração de α-glucosidase neutra e um aumento nos defeitos da cauda, ocorre devido a alterações no estilo de vida. A capacidade antioxidante total das células e as variações ao nível da oxidação proteica demonstram também ser dependentes do consumo de alcool e tabaco. Foram também verificadas algumas correlações entre os parâmetros analisados que poderão ser importantes numa perspetiva clínica. Concluindo, alterações no estilo de vida são responsáveis pela diminuição da qualidade seminal e pelo aumento de modificações proteicas, o que pode levar consequentemente a um decréscimo do potencial de fertilização.
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Zhang, Wei. "Differential Impact of Age and Stress on Amygdala Physiology and Function." Thesis, Rosalind Franklin University of Medicine and Science, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3566591.
Повний текст джерелаАнотація:
Occasional stress is a normal aspect of mammalian life. However repeated or prolonged stress exposure dysregulates stress responses and contributes to the onset or exacerbation of affective disorders such as anxiety, depression and post-traumatic stress disorder (PTSD). Understanding the underlying mechanism of the effect of stress on affective behaviors is essential for effective prevention and treatment of these disorders.
All affective disorders share a deficit in the regulation of emotion. The amygdala plays crucial role in this regulation and is adversely affected by stress. This suggests that stress precipitates abnormal affective state by altering amygdala function. While the effect of acute stress on the amygdala has been well described, less is know about the impact of repeated stress nor its age-dependency. We hypothesized that repeated stress leads to a hyperactive amygdala and impairs the amygdala function in regulating affective behaviors, and such impacts are greater during prepubescence than during adulthood. In this study, we subjected prepubescent (postnatal day, PND ∼30) and adult rats (PND ∼65) to repeated restraint stress. We then measured the effect of stress on amygdala physiology and amygdala-dependent behavior in prepubescent (PND ∼40) and adult (PND ∼75) rats. The results were compared between age-matched non-restraint and repeated restraint groups and across age. Repeated restraint stress increased basolateral amygdala (BLA) spontaneous population activity in prepubescent rats whereas it enhanced individual neuron activity in adult rats. In parallel with these physiological changes, repeated restraint stress enhanced initial expression of conditioned fear in both age groups, but impaired within session fear extinction only in prepubescent rats. Further studies demonstrated that repeated restraint stress reduced the BLA projection neuron inhibition by exogenous GABA in prepubescent rats. However, repeated restraint stress enhanced the BLA projection neuron excitation by exogenous glutamate in adult rats. In addition, repeated restraint reduced basal GABA transmission and enhanced mPFC-induced excitation of spontaneously active BLA projection neurons in both age groups. Together, these findings indicate that repeated restraint results in a generalized hyperactive and hyper-responsive amygdala. The distinct changes in amygdala physiology at different developmental stages might underlie age-dependent effect of stress on affective behaviors. Overall, this study leads to a better understanding of the pathophysiology of stress-related affective disorders and provide insight into age-specific treatment of these disorders.
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Conklin, Brian Scott. "The effects of fluid shear stress on endothelial cell barrier function." Diss., Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/17221.
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Oosthuyzen, Wilna. "Coping, stress hormones and cardiovascular function in urbanised Africans / Wilna Oosthuyzen." Thesis, North-West University, 2007. http://hdl.handle.net/10394/1434.
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Bains, Rasneer. "The effect of stress and anxiety on rat brain mitochondrial function." Thesis, University of Sunderland, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555649.
Повний текст джерелаАнотація:
Mitochondria play a major role in the maintaining the cellular homeostasis, it is therefore to be expected that if this homeostasis is challenged, the mitochondria would be among the first to respond. Since homeostasis is essential to survival, the stress response achieves what is termed as "ALLOSTASIS" which can be defined as the process of maintaining homeostasis by active means, through the release of stress response mediators. Depression has been described as a representation of the activation of primary stress mediators. This thesis explores the effect of stress on neuronal energy metabolism. To achieve this, various experimental studies were designed to encompass a variety of stimuli; e.g. age, anxiety, inflammation and physiological stress i.e. elevated serum corticosterone. Mitochondria were prepared using differential centrifugation through 18% (v/v) percoll density gradient. To establish a sound base on which the study was to be based the mitochondrial preparation was validated using respiratory control index (RCI), marker enzymes and electron micrographs, and compared to various other studies using the same technique for preparation. The preparation used in this study was demonstrably superior in purity and function. Initial studies dealt with age and anxiety as sources of stress. It was demonstrated that older rats (24months+) have lower (20-25%) baseline mitochondrial function as compared to young animals (2-3 months). When exposed to anxiety, young animals demonstrated a transient decline in mitochondrial function seen as a fall in RCI, but older animals showed an inhibitory effect on Complex 11 of the mitochondrial respiratory chain which was seen as a significant (P<0.01) decrease in reactive oxygen species (ROS) production in the presence of 5 mM succinate but not 5 mM glutamate plus 5 mM malate (G+M). This could be attributable to the phenomenon of partial uncoupling, a protective mechanism that stems the production of large amounts of ROS in stressed mitochondria by lowering the membrane potential, and the consequent loss of reverse electron transfer that is responsible for the large amounts of ROS being produced at complex I in the presence of a complex 11 substrate. lnterleukin-tp (IL-1P) was found to block the improvement of brain mitochondrial function resulting from exposure to brain derived neurotropic factor (BDNF; 333 ng rnl"). This effect was found to be concentration-dependent. IL-1 p was seen to have no effect on the mitochondrial function in the absence of BDNF. An earlier study by this laboratory had shown the involvement of RAS/MAPK pathway in the mitochondrial propagation of the signal initiated by BDNF. IL-1 P was seen to interfere with this pathway at the site of scaffolding proteins that are essential for MAPK docking and therefore for signal propagation. Using an in vivo model of chronic stress involving oral corticosterone (0.5%) in drinking water for 14 days was developed. This model showed successfully that chronic exposure significantly reduced the RCI of treated animals from 8.70 ± 0.30 to 7.17 ± 0.17 for G+M and from 7.56 ± 0.60 to 5.50 ± 0.20 for succinate (P<0.05; n=5). To further validate the model, daily water consumption and weight gain charts were maintained and they showed that there was no significant variation between the treated and the untreated group. This model was then used to simulate chronic stress induced depression in subsequent studies. The prototypes of the three generations of antidepressants: imipramine for 1st generation, fluoxetine for 2nd generation and tianeptine for the novel agents or 3'd generation, were used in subsequent in vivo experiments designed to study the effect of stress and antidepressant therapy on mitochondrial function expressed in terms of RCI, ROS production and the effect on serum corticosterone through a quantitative enzyme immunoassay. The main findings of the in vivo studies were that imipramine acts primarily through a corticosterone- dependent pathway because it significantly lowered serum corticosterone concentration in corticosterone treated animals. However its effects on the mitochondrial function were not significant. Fluoxetine was found to have no effect on mitochondrial function, either in vitro or in vivo. Tianeptine was found to have an effect on the mitochondrial function in vitro but not in vivo. This study has identified a potential pivotal role for mitochondria in relation to the manifestation of stress responses, regardless of the origin of the stressor.
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Gerber, Robert Thomas. "Vascular function and oxidative stress in diabetic pregnant and the offspring." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322205.
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Wilson, Stacey J. "The effect of heat stress on ovarian function in dairy cattle /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9842573.
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Bueler, Stephanie A. "A pro-survival function of caspase-8 in stress-induced apoptosis /." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97915.
Повний текст джерелаАнотація:
Apoptosis is a genetically programmed form of cell death that plays an essential role in the tissue homeostasis and development of multicellular organisms. Apoptotic cellular suicide is tightly regulated by both pro-apoptotic and anti-apoptotic proteins. The dysregulation of apoptosis manifests in a number of pathologies, such as cancer, autoimmunity and neurodegenerative disorders. Thus further insight into these mechanisms may provide a basis for therapeutic opportunities. The primary executioners of cell death belong to a family of cysteine proteases known as caspases that cleave numerous substrates resulting in the morphological characteristics of apoptosis. Caspase8 is the apical caspase involved in death receptor-mediated apoptosis, which upon activation can cleave downstream executioner caspases-3, -6, and -7. Interestingly, in humans, a deficiency in caspase-8 impairs lymphocyte activation and proliferation.Apoptotic signaling can be effectively blocked by Inhibitor of Apoptosis Proteins (IAPs), of which the X-linked Inhibitor of Apoptosis Protein (XIAP) is the best characterized. XIAP exerts it's anti-apoptotic effect by binding to caspases-3, -7, and -9, thus preventing their activation.
In an attempt to characterize the function of caspase-8 in stress-induced apoptosis, RNA interference was employed to effectively and functionally silence caspase-8 in HeLa cells. Cells transfected with caspase-8-specifc siRNA were subsequently treated with the drug staurosporine, a general protein kinase inhibitor known to induce apoptosis via cell stress. Counter-intuitively, cells in which caspase-8 had been silenced exhibited increased cell death in response to staurosporine. I have shown that the increased sensitization to death in these cells may be ascribed to a concomitant decrease in XIAP protein levels due to increased degradation via the proteasome. The ability of caspase-8 to maintain the protein levels of XIAP was not a function of caspase-8's enzymatic activity, but may be attributed to a non-enzyme function of the protein. Collectively, these findings suggest that caspase-8 may provide a pro-survival signal through the maintenance and stabilization of an anti-apoptotic protein, XIAP, in response to staurosporine-induced apoptosis, and that this anti-apoptotic function of caspase-8 is irrespective of it's pro-apoptotic enzymatic activity.
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Huggett, Brett Andrew. "The Plant Vascular System: Structure, Function, and Responses to Environmental Stress." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10913.
Повний текст джерелаАнотація:
Environmental stressors such as nutrient deficiency and insect infestation can significantly impact tree health. Despite much research on the ecological effect on forests in the northeastern United States due to calcium depletion and hemlock woolly adelgid infestation, little is known regarding the physiological mechanisms altered by these stress factors. I tested the hypothesis that calcium depletion, associated with sugar maple decline, compromises water transport processes as a result of calcium-related reductions in cell growth and stabilization. A survey of forest-grown sugar maples from a long-term replicated calcium-manipulation study showed no significant impact of calcium deficiency on wood density, stem hydraulic conductivity (Ks), or vulnerability to cavitation (VC). In vitro removal of xylem-bound calcium showed no impact on VC or air seeding thresholds (Pt). Results suggest that sugar maple decline is not caused by compromises in xylem function due to calcium deficiency. I also tested the hypothesis that hemlock woolly adelgid (Adelges tsugae Annand) (HWA) infestations impact water transport processes and nutrient partitioning in eastern hemlock trees. HWA infestation resulted in higher Ks due to an increase in average tracheid lumen area associated with the proliferation of false rings. HWA-infested trees exhibited higher rates of net photosynthesis and significant changes in foliar nutrient partitioning. These results are the first to demonstrate increases in Ks and alterations in foliar cation levels in response to HWA infestation. In two additional studies, I investigated methods for evaluating the structure and function of xylem networks. Using sequential sectioning of aerial roots of epiphytic aroids, I directly quantified the topographic relation of vessels in a single organ with measurements of vessel length, diameter, vessel end overlap length, and vessel stelar orientation. In a separate study, I explored the relationship between vessel length and measurements of Pt. In establishing guidelines for estimating whole-stem cavitation with the use of single vessel air injection, I demonstrate that calculations of Pt are influenced by stem length measured and removal of native emboli prior to testing. Improvements in tools to quantify xylem structure and function will enhance our ability to understand the responses of forest trees to environmental stress.
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Rochette, Lynn M. "Resting Hemodynamic Function and Reactivity to Acute Stress: The Influence of Hydration on Cardiac Function and Plasma Volume." Ohio University / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1108392572.
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Rochette, Lynne M. "Resting hemodynamic function and reactivity to acute stress : the influence of hydration on cardiac function and plasma volume /." Ohio : Ohio University, 2004. http://www.ohiolink.edu/etd/view.cgi?ohiou1108392572.
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Bush, Victoria. "Role of neonatal corticosterone on subsequent serotonergic neuronal development and brain function in adult rats." Thesis, Nottingham Trent University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272812.
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Keita, Åsa. "Barrier function of the Follicle-Associated Epithelium in Stress and Crohn's disease." Doctoral thesis, Linköpings universitet, Kirurgi, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-9271.
Повний текст джерелаАнотація:
Crohns sjukdom är en kronisk inflammatorisk tarmsjukdom av okänd orsak. Det tidigaste tecknet på Crohns sjukdom är mikroskopiska sår i det s.k. follikelassocierade epitelet (FAE) som täcker ansamlingar av immunceller i tarmen. FAE är specialiserat för att fånga innehåll från tarmen och transportera det till underliggande immunvävnad. Denna funktion är viktig för att inducera skyddande immunsvar, men den utgör också en ingångsväg för sjukdomsalstrande bakterier. Crohns sjukdom är associerat med ett kraftigt ökat immunsvar mot bakterier, och sjukdomsförloppet kan ändras av stress. Det övergripande syftet med avhandlingen var att studera effekterna av stress på FAE samt att undersöka rollen av FAE vid utvecklingen av tarminflammation, särskilt vid Crohns sjukdom. Inledningsvis studerades effekterna av psykologisk stress på FAE. Stressade råttor uppvisade ökad genomsläpplighet av bakterier efter stress, och passagen var högre i FAE än i vanligt epitel. Efterföljande experiment visade att stressförändringarna i slemhinnan regleras via kortikotropinfrisättande hormon och mastceller. Vidare visade det sig att vasoaktiv intestinal peptid kunde efterlikna stressens effekter på genomsläppligheten, och att detta kunde förhindras genom att blockera mastcellerna. Studier av tunntarmsslemhinna från patienter med icke-inflammatorisk tarmsjukdom och friska kontroller visade en högre passage av bakterier i FAE än i vanligt epitel. Hos patienter med Crohns sjukdom var bakteriepassagen genom FAE betydligt ökad jämfört med kontroller. Resultaten från detta avhandlingsarbete visar att stress kan förändra upptaget av bakterier från tarmen via FAE, med mekanismer som innefattar kortikotropinfrisättande hormon och mastceller. Detta har gett nya kunskaper kring regleringen av slemhinnebarriären. Vidare presenterar denna avhandling nya insikter i sjukdomsuppkomsten vid Crohns sjukdom genom att påvisa en tidigare okänd defekt i barriärfunktionen i FAE.The earliest observable signs of Crohn’s disease are microscopic erosions in the follicle-associated epithelium (FAE) covering the Peyer’s patches. The FAE, which contains M cells, is specialised in sampling of luminal content and delivery to underlying immune cells. This sampling is crucial for induction of protective immune responses, but it also provides a route of entry for microorganisms into the mucosa. Crohn’s disease is associated with an increased immune response to bacteria, and the disease course can be altered by stress. The overall aim of this thesis was to study the effects of stress on the FAE and elucidate the role of FAE in the development of intestinal inflammation, specifically Crohn’s disease. Initially, rats were submitted to acute and chronic water avoidance stress to study the effects of psychological stress on the FAE. Stressed rats showed enhanced antigen and bacterial passage, and the passage was higher in FAE than in regular villus epithelium (VE). Further, stress gave rise to ultrastructural changes. Subsequent experiments revealed the stress-induced increase in permeability to be regulated by corticotropin-releasing hormone and mast cells. Furthermore, vasoactive intestinal peptide (VIP) mimicked the stress effects on permeability, and the VIP effects were inhibited by a mast cell stabiliser. Human studies of ileal mucosa from patients with non-inflammatory disease and healthy controls showed a higher antigen and bacterial passage in FAE than in VE. In patients with Crohn’s disease, the bacterial passage across the FAE was significantly increased compared to non-inflammatory and inflammatory controls (ulcerative colitis). Furthermore, there was an enhanced uptake of bacteria into dendritic cells, and augmented TNF-α release in Crohn’s disease mucosa. Taken together this thesis shows that stress can modulate the uptake of luminal antigens and bacteria via the FAE, through mechanisms involving CRH and mast cells. It further shows that human ileal FAE is functionally distinct from VE, and that Crohn’s disease patients exhibit enhanced FAE permeability compared to inflammatory and non-inflammatory controls. This thesis presents novel insights into regulation of the FAE barrier, as well as into the pathophysiology of Crohn’s disease by demonstrating a previously unrecognised defect of the FAE barrier function in ileal Crohn’s disease.
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Yang, Huei-Hsin Clarice. "Oxidative stress compromises vasomotor function of the thoracic aorta in Marfan Syndrome." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/15003.
Повний текст джерелаАнотація:
Introduction: Marfan syndrome is an autosomal dominant connective tissue disorder that causes life-threatening cardiovascular complications such as thoracic aortic dilatation and aneurysm. We
have demonstrated that Marfan syndrome compromises contractile function of the aorta and impairs nitric oxide-mediated relaxation. We hypothesize that oxidative stress impairs contractility and endothelium-dependent relaxation in the thoracic aorta of Marfan mice. Methods: Adrenergic contractions and cholinergic relaxations of thoracic aorta from mice heterozygous for FBN1 allele (Fbn1C¹⁰³⁹G/+ , n=40; age=3,6,9 months), a well-defined model of Marfan syndrome, were compared with those from control littermates (n=40). Results: At 3 and 6 months, oxidative stress, as indicated by the plasma 8-isoprostane level, was 50% greater in the Marfan group than in the control. In 9 months old Marfan mice, the depressed phenylephrine-induced contraction was normalized by the preincubation of superoxide dismutase (SOD) which increased the maximal contractile response (Emax) and pEC₅₀ for phenylephrine-stimulated contraction by 91% and 2.75-fold. The compromised endothelial function was also restored by SOD which increased the sensitivity to acetylcholine by 10.7 and
12.3-fold at 3 and 6 months, respectively. Such improvement was absent in the controls. In 9 months old Marfan mice, the phenylephrine-contraction was potentiated 141% by 1400W, an inducible nitric oxide synthase (iNOS) inhibitor. The pEC₅₀ was normalized by 1400W and allopurinol, an inhibitor of xanthine oxidase. In the same group, both Emax and pEC₅₀ of
acetyicholine was normalized by apocynin, an inhibitor of NAD(P)H oxidase. Protein expression of SOD was decreased at 3 and 9 months in the Marfan group, whereas expression of xanthine oxidase, iNOS, gp9lphox, p47phox and p67phox, the subunits of NAD(P)H oxidase, was all increased.
Conclusions: The compromised vasomotor function in Marfan thoracic aorta could be associated with oxidative stress resulting from decreased expression of SOD and increased expression of iNOS, xanthine oxidase, and NAD(P)H oxidase.
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Keita, Åsa. "Barrier function of the follicle-associated epithelium in stress and Crohn's disease /." Linköping : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-9271.
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Loganathan, Arunan. "Relationship between Human Instestinal Permeability and Potassium Channel Function during Metabolic Stress." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.507636.
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