Thèses : « Cardak »

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Essandoh, Kobina. « The Role of Tsg101 in the Development of Physiological Cardiac Hypertrophy and Cardio-Protection from Endotoxin-Induced Cardiac Dysfunction ». University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1563526987921154.

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Shimamoto, Tomonari. « Dispatcher instruction of chest compression-only CPR increases actual provision of bystander CPR ». Kyoto University, 2018. http://hdl.handle.net/2433/232308.

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Middleton, Natalie. « The acute impact of single and repeated bouts of prolonged exercise on cardiac function and cardio-biomarker release ». Thesis, Brunel University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435756.

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Mattsson, C. Mikael. « Physiology of Adventure Racing : with emphasis on circulatory response and cardiac fatigue ». Doctoral thesis, Gymnastik- och idrottshögskolan, GIH, Björn Ekbloms och Mats Börjessons forskningsgrupp, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:gih:diva-1754.

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The overall aims of this thesis were to elucidate the circulatory responses to ultra-endurance exercise (Adventure Racing), and furthermore, to contribute to the clarification of the so called “exercise-induced cardiac fatigue” in relation to said exercise. An Adventure race (AR) varies in duration from six hours to over six days, in which the participants have to navigate through a number of check-points over a pre-set course, using a combination of three or more endurance/outdoor sports, e.g., cycling, running, and kayaking. This thesis is based on the results from four different protocols; 12- and 24-h (n = 8 and 9, respectively) in a controlled setting with fixed exercise intensity, and 53-h and 5-7-day (n = 15 in each) in field setting under race conditions. The subjects in all protocols were experienced adventure racing athletes, competitive at elite level. Study I and II address the circulatory responses and cardiovascular drift, using methods for monitoring heart rate (HR), oxygen uptake (VO2), cardiac output (non-invasive re-breathing) and blood pressure, during ergometer cycling at fixed steady state work rate at periods before, during and after the ultra-endurance exercise. In Study III and IV we examined the possible presence of exercise-induced cardiac fatigue after a 5-7-day AR, from two different perspectives. In Study III analyses were performed with biochemical methods to determine circulating levels of cardiac specific biomarkers (i.e., creatine kinase isoenzyme MB (CK-MB), troponin I, B-type natriuretic peptide (BNP) and N-terminal prohormonal B-type natriuretic peptide (NT-proBNP)). We also made an attempt to relate increases in biomarkers to rated relative performance. In Study IV we used tissue velocity imaging (TVI) (VIVID I, GE VingMed Ultrasound, Norway) to determine whether the high workload (extreme duration) would induce signs of functional cardiac fatigue similar to those that occur in skeletal muscle, i.e., decreased peak systolic velocities. Using conventional echocardiography we also evaluated whether the hearts of experienced ultra-endurance athletes are larger than the normal upper limit. The central circulation changed in several steps in response to ultra-endurance exercise. Compared to initial levels, VO2 was increased at every time-point measured. The increase was attributed to peripheral adaptations, confirmed by a close correlation between change in VO2 and change in arteriovenous oxygen difference. The first step of the circulatory response was typical of normal (early) cardiovascular drift, with increased HR and concomitantly decreased stroke volume (SV) and oxygen pulse (VO2/HR), occurring over the first 4-6 h. The second step, which continued until approximately 12h, included reversed HR-drift, with normalisation of SV and VO2/HR. When exercise continued for 50 h a late cardiovascular drift was noted, characterised by increased VO2/HR, (indicating more efficient energy distribution), decreased peripheral resistance, increased SV, and decreased work of the heart. Since cardiac output was maintained at all-time points we interpret the changes as physiologically appropriate adaptations. Our findings in Study III point towards a distinction between the clinical/pathological and the physiological/exercise-induced release of cardiac biomarkers. The results imply that troponin and CKMB lack relevance in the (healthy) exercise setting, but that BNP, or NT-proBNP adjusted for exercise duration, might be a relevant indicator for impairment of exercise performance. High levels of NTproBNP, up to 2500 ng · l -1 , can be present after ultra-endurance exercise in healthy athletes without any subjective signs or clinical symptoms of heart failure. However, these high levels of NT-proBNP seemed to be associated with decreased relative exercise performance, and might be an indicator of the cardiac fatigue that has previously been described after endurance exercise. Study IV revealed that the sizes of the hearts (left ventricle) of all of our ultra-endurance athletes were within normal limits. The measurements of peak systolic velocities showed (for group average) no signs of cardiac fatigue even after 6 days of continuous exercise. This discrepancy between ours and other studies, involving e.g., marathon or triathlon, might reflect the fact that this type of exercise is performed at relatively low average intensity, suggesting that the intensity, rather than the duration, of exercise is the primary determinant of cardiac fatigue.
Physiology of Adventure Racing

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Wu, Chun Andy, et 胡俊. « The effectiveness of dispatcher-assisted cardio-pulmonary resuscitation on survival of out-of-hospital cardiac arrest : a literature review ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48426507.

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Background According to data from Department of Health, in 2011 heart diseases was the second commonest leading cause of death in Hong Kong [13]. Shortening the time from cardiac arrest to Cardio-pulmonary Resuscitation (CPR) could increase the chance of survival. If the brain of the patient who suffers from cardiac arrest does not receive oxygen within 4 minutes, severe brain damage might occur [14]. In some countries like US and Finland, dispatcher will give CPR instruction to caller when cardiac arrest is recognized. Therefore, the patient could receive early CPR before the arrival of paramedics. If dispatcher-assisted CPR is implemented in Hong Kong, the chance of survival of out-of-hospital cardiac arrest (OHCA) patient could be increased. Objective 1. To evaluate whether it is evident that dispatcher-assisted CPR and dispatcher instruction [22] would improve survival of OHCA. 2. To evaluate whether these measures could be implemented in Hong Kong. Data Source PubMed was searched for articles in English language with no limit set for time of the study. The keywords were dispatcher-assisted CPR and out of hospital. No inclusion criteria were set on the publication type and other details. Results Initial PubMed search resulted in 24 articles. After reviewing the abstracts, 10 articles were selected for full-text assessment. Finally, four relevant articles were selected for the literature review. Of the four papers, two were retrospective cohort studies; one was before-after comparison study while the remaining one was randomized control trial. Three papers (Rea et al, Eisenberg et al, and Kuisma et al.) used the survival to hospital discharge as the effect measure for the primary outcome to evaluate the effectiveness of dispatcher-assisted CPR. The remaining paper (Hallstrom et al.) mainly studied the potential benefit and harm from dispatcher-assisted CPR. Using no bystander CPR as the reference group, the multivariate adjusted odds ratio of survival was 1.45 (95% CI, 1.21, 1.73) for dispatcher-assisted bystander CPR and 1.69 (95% CI, 1.42, 2.01) for bystander CPR without dispatcher assistance [2]. The percentage of total bystander-initiated CPR increased from 45% to 56% after the programme (difference: 11.1%, 95% CI, ±9.3%). Besides, the percentage discharged for dispatcher-assisted CPR group after the programme was 15% higher than that before the programme [6]. The most important findings are related to the number of cardiac arrest calls in that when the dispatcher handled on less than 4 Ventricular Fibrillation (VF) calls during the study period, the survival to hospital discharge was 22.1% compared to 38.2% and 39.4% when the dispatcher handled 4 to 9 calls or more than 9 calls (p = 0.0227 for the three groups) [8]. With telephone guided CPR, the survival to hospital discharge was 43.1% compared with 31.7% when CPR instructions were not provided (p = 0.0453) [8]. In patients (n = 3,320) receiving advanced cardiac life support (ACLS) a total of 993 (29.9%) was found to be benefited from dispatcher-assisted CPR [7]. Conclusion Instructions by dispatcher can improve bystander CPR rates, which in turn increases the chance of survival [26]. Dispatcher-assisted CPR is worth considering to be recommended to all callers reporting a patient in cardiac arrest in Hong Kong.
published_or_final_version
Public Health
Master
Master of Public Health

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Gibbison, Ben. « Activation of the hypothalamic-pituitary-adrenal axis during cardiac surgery : the effect of surgical stress and cardio-pulmonary bypass ». Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.652032.

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Glucocorticoids form an essential part of the response to major surgery and critical illness. Both inappropriately low and excessively high levels of glucocorticoid in this context lead to raised morbidity and mortality. Controversy still exists over who these patients are, how they might be diagnosed and when, how and what to treat them with. Simple control of endogenous glucocorticoids is well known and is regulated by a negative feedback system comprising the hypothalamus, the pituitary and the adrenal gland (the HPA axis). It is widely known that cortisol is secreted in a diurnal rhythm; levels are low during periods of sleep and rise to a peak just before waking. Underlying this diurnal rhythm is an ultradian rhythm of discrete pulses. It was previously thought that these pulses were due to a 'pulse generator'. However, recent work has shown that it is inherent within the system and as a result of the feedforward-feedback properties of adreno-corticotrophic hormone (ACTH) and cortisol. Pulsatility is important; transcription of cortisol responsive genes 'pulse' in-time with pulses of cortisol and non-pulsatile cortisol replacement in those with absolute deficiency is associated with an excess mortality. No previous study has examined ultradian rhythms of cortisol at and around the time of major surgery. Coronary artery surgery can be performed with (on-pump) or without (offpump) the use of cardiopulmonary bypass (CPB). Off-pump surgery is associated with lower levels of systemic inflammation as measured by markers, although this does not translate into improved long-term outcomes. Previous work using point measures of cortisol and ACTH after cardiac surgery has shown that both cortisol and ACTH rise by the end of surgery, with cortisol remaining elevated, but ACTH being 'suppressed' by 24 hours post surgery - a so called 'disconnect' between the pituitary and adrenal glands.

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Hatakeyama, Toshihiro. « A smartphone application to reduce the time to AED delivery after a witnessed out-of-hospital cardiac arrest : a randomized simulation-based study ». Kyoto University, 2018. http://hdl.handle.net/2433/233835.

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McDonald, Cameron. « Investigations in Cardiac Development and Cardiac Regeneration ». Thesis, Griffith University, 2009. http://hdl.handle.net/10072/366063.

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Cardiovascular disease and congenital heart disease impose a massive burden on society around the world. From the cost in terms of lost human lives and diminished quality of life, to the financial expense of ongoing medical treatment, the heart’s inability to effectively repair and regenerate itself presents a major challenge for medical research. The research conducted within this thesis hoped to contribute to our knowledge of the molecular pathways of myocardial development, and to explore the potential of olfactory derived stem cells to repopulate insulted myocardium. A combination of molecular biology and classical embryology techniques were first used to characterise two novel cDNAs identified in an earlier study as being upregulated in the regions of cardiac development within the chick embryo. cDNA and genomic library screening along with RACE (rapid amplification of cDNA ends) produced products which were sequenced to identify both the transcript and genomic sequence for both of the genes. Protein expression constructs were then used to identify the localisation of the encoded proteins, and whole mount in situ hybridisation utilised to identify the temporal and spatial expression patterns of the genes. The first cDNA was identified as the vertebrate homologue of the Drosophila e(y)2 gene, and produces a transcript of approximately 600 bp in the chick with a genomic structure consisting of 5 exons covering approximately 6 Kb. The encoded protein localises to the nucleus. Its expression is ubiquitous both temporally and spatially, which is at odds with its initial method of identification. The second cDNA remains novel at the time of submission, and shows no homology to any characterised genes. This cDNA, named C1-3C, produces two alternative transcripts, one of approximately 700 bp, and a second of 9.9 Kb, with a genomic structure showing no introns within the 2 Kb of analysed sequence. The encoded protein again localises to the nucleus. Expression of the C1-3C gene demonstrated a discrete pattern, though this pattern is again contrary to an up-regulation within the cardiogenic regions. Whilst unfortunately neither of the investigated genes appear to play a direct role in cardiac development, the aim of characterisation of these novel cDNAs was achieved.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Jakovljevic, Djordje. « The effect of specific interventions on cardiac power output and selected cardio-respiratory variables in patients with mild to severe heart failure ». Thesis, Bucks New University, 2009. http://bucks.collections.crest.ac.uk/9797/.

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Cardiac power output is a central haemodynamic measure which describes pumping capability and performance of the heart. This is a unique measure as it accounts for both, flow- and pressure-generating capacities of the heart. Cardiac power output (CPO) is calculated from mean arterial pressure and cardiac output. Popular noninvasive methods for cardiac output measurement today include rebreathing methods. From the practical and clinical perspective it is important to know which of the commonly measured cardio-respiratory variables, obtained from a cardiopulmonary exercise test, are good predictors of peak CPO in healthy but also in heart failure populations. Until now there has been no measurement of cardiac power output in patients implanted with a left ventricular assist device (LVAD) and those explanted (recovered) patients. In a comparison study design it has been shown that peak cardiac power output differentiates well during cardiac restoration using LVADs and emphasizes the benefits of this therapy. It seems that CPO has the potential to be a key physiological marker of heart failure severity and can guide the management of LVAD patients. Furthermore as a consequence of acute reduction of LVAD support, there is a decrease in cardiac pumping capability and exercise performance. A decrease at rest and at peak exercise, expressed in percentages, was higher in central haemodynamics, particularly in CPO, than in the conventionally measured peak oxygen consumption. This suggests that CPO is more sensitive to acute reduction of LVAD support than oxygen consumption. In patients with severe heart failure and those implanted with an LVAD, the relationship between peak CPO and peak oxygen consumption is only modest. In healthy adults and LVAD explanted patients this relationship was high. No strong relationship was found between peak CPO and anaerobic threshold, circulatory power, oxygen pulse or ventilatory efficiency in LVAD implanted and patients with severe heart failure. Finally, regarding di fferent modalities of exercise training, in contrast with resistance training, aerobic exercise training may increase both maximal flow-generating capacity of the heart and peak oxygen consumption and also delays anaerobic metabolism in patients with stable chronic heart failure. Improved peak oxygen consumption, following aerobic exercise training, is closely associated with an exercise-induce increase in cardiac output.

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Paul, Ashok Abraham. « Investigation of cardiac and non-cardiac drugs that modulate cardiac Herg Kâº channels ». Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274632.

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Baily, James Edward. « Role of cardiac perivascular cells in cardiac repair ». Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15846.

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Ischaemic heart disease accounts for approximately 7 million deaths worldwide on a yearly basis and this figure is only set to rise as life expectancy in developing countries increases. Although no longer considered a post mitotic organ, the adult heart demonstrates only a very limited capacity for regeneration. Consequently ischaemic injury results in massive loss of contractile cardiomyocytes with damaged myocardium replaced by a non-contractile and poorly conductive collagen scar. This in turn often leads to the development of heart failure. Enhancing or supplementing the myocardial regenerative capacity of the heart is thus a key goal in the development of effective therapies for the treatment of cardiac infarction. Several stem cell populations of non-cardiac origin have been investigated for their capacity to contribute to myocardial repair when therapeutically transplanted into injured hearts. Recent efforts have focused on the “next generation” of donor cells, endogenous cardiac progenitor cells, as these are thought to be better adapted to survival in the cardiac environment and to possess enhanced cardiomyocyte differentiation potential. Pericytes, proposed as the source of the elusive mesenchymal stem cells (MSC) within multiple tissues, are a potential new cell type for use in regenerative medicine. This study tests the hypothesis that pericytes and another perivascular progenitor population, the adventitial cell, from foetal cardiac tissue will positively contribute to the repair of the myocardium post injury. Staining of human foetal ventricular myocardium confirmed the presence of large numbers of both cell types with pericytes tightly associated with capillaries and adventitial cells primarily located in the outer, adventitial layer of muscular arteries. CD146+ CD34- pericytes and CD146- CD34+ adventitial cells were isolated by FACS and expanded in culture. On examination of gene and protein expression both populations stably expressed a similar panel of pericyte markers, MSC markers and cardiac transcription factors as well as c-kit, a cardiac progenitor cell candidate marker. Co-culture with neo-natal rat cardiomyocytes induced expression of an additional cardiac progenitor marker Isl-1 and a mature cardiomyocyte marker ANP in adventitial cells but not pericytes. Labelled, co-cultured, perivascular progenitors readily adhered to rat cells but did not appear to contract independently. De-methylation of perivascular progenitors prior to co-culture resulted in expression of sarcomeric proteins and spontaneous cytoplasmic calcium fluctuations in both populations but more commonly in pericytes. This suggests that cardiac perivascular cells contain a minor sub-population capable of cardiomyocyte differentiation. When these populations were injected into the infarcted hearts of NOD/SCID mice, the animals treated with adventitial cells had significantly reduced cardiac function at 21 days post-surgery on ultrasound examination. An increased scar area and a non-significant trend towards increased scar length and a decreased wall thickness were also observed. Transplanted cells of both groups were detected in low numbers 21 days after injection. Adventitial cells were retained much more readily and in both populations retained cells exhibited three key morphologies: fibroblast type; macrophage type; and cardiomyocyte type. The majority of cells adopted a fibroblast type morphology, lesser numbers a macrophage like morphology and only rare cells a cardiomyocyte like morphology. Both fibroblast and cardiomyocyte type cells had single, human nuclear antigen positive nuclei suggesting true differentiation rather than cell fusion and pericytes exhibited an enhanced ability to differentiate into cardiomyocytes. This supports the in-vitro findings of a minor pro-cardiomyogenic subset within the perivascular cell population. As a result of these findings the starting hypothesis was modified to propose that perivascular cells play a significant role in cardiac fibrosis, largely mediated through expression of surface integrin receptors. This was tested using mice expressing fluorescent proteins under the control of the PDGFR-β promoter and mice in which the αv integrin subunit, common to 5 integrin receptors, had been deleted on the surface of PDGFR-β+ cells. Immunostaining and flow cytometry revealed the PDGFR-β expression to be tightly restricted to perivascular cells and co-expressed with the fibroblast markers, vimentin, PDGFR-α, CD90.2 and CD34 in a subset of cells. Cardiac fibroblasts isolated from reporter mouse hearts revealed strong expression of PDGFR-α and CD34 but PDGFR-β expression in only approximately 20% of the population on flow cytometry. Following angiotensin II induced cardiac hypertrophy and fibrosis approximately 50% of fibroblasts expanding the interstitium were PDGFR-β+. Genetic deletion of the αv integrin subunit on PDGFR-β+ cells resulted in a reduction in cardiac interstitial collagen content of about 50% compared to wild type controls. These findings suggest that the cardiac perivascular PDGFR-β+ population is heterogeneous with a sub-population likely to be fibroblasts or fibroblast progenitors and that the development of cardiac interstitial fibrosis is in part modulated by integrin receptor expression on these cells. In summary this study provides evidence of the existence of a pro-fibrotic progenitor population, which co-express pericyte and MSC markers, within the cardiac perivascular niche. These cells contribute to cardiac fibrosis both on transplantation and endogenously following cardiac injury with the latter mediated via αv integrin expression. Within the perivascular progenitor population however there also appears to be a minor subset of pro-cardiomyogenic cells which are able to adopt a cardiomyocyte phenotype both in-vitro and in-vivo.

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Dumas, Florence. « Analyse de l’influence des interventions thérapeutiques précoces au sein d’une cohorte de patients survivants d’arrêt cardio-respiratoire ». Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05S006/document.

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Position du problème. L’arrêt cardiaque extra-hospitalier (ACEH), dont la forme clinique la plus caricaturale correspond à la « mort subite », représenterait la première cause de mortalité à travers le monde. Malgré les améliorations apportées à leur prise en charge, le pronostic de ces patients demeure très péjoratif, y compris chez ceux qui ont bénéficié d’une réanimation initiale avec succès. En effet, la longue période d’ischémie suivie du phénomène de reperfusion secondaire au retour d’une activité circulatoire (RACS) est à l’origine d’une cascade de phénomènes physiopathologiques qui caractérisent le syndrome post-arrêt cardiaque. Plusieurs éléments thérapeutiques, telles que la reperfusion coronaire précoce et l’hypothermie thérapeutique, se sont développés ces dernières années afin de diminuer la morbi-mortalité importante observée dans cette situation. L’intérêt de ces interventions précoces sur le pronostic ultérieur demeure cependant débattu, car il a souvent été établi sur des sous-groupes de patients très sélectionnés. Objectif. L’objectif de ce travail était d’évaluer l’influence de ces interventions thérapeutiques précoces sur le devenir des patients victimes d’ACEH et admis vivants en service de réanimation. Méthode. Depuis 2000, une cohorte de patients survivants d’ACR et admis vivants en réanimation a été constituée dans un centre spécialisé. L’ensemble des caractéristiques démographiques, pré-hospitalières et hospitalières ont été analysées. L’analyse multivariée des facteurs pronostiques dans cette cohorte a utilisé principalement les méthodes de régression logistique. Résultats principaux. Entre 2003 et 2008, 435 patients ont été admis, ne présentaient pas d’étiologie extra-cardiaque évidente et ont bénéficié d’une coronarographie immédiate et systématique. Une lésion coronaire récente a été observée chez près de la moitié d’entre eux. Les moyens de détection d’une étiologie cardiaque sont extrêmement limités que ce soit par des modèles prédictifs simples utilisant des paramètres démographiques ou circonstancielles ou par des paramètres para-cliniques tels que l’électrocardiogramme ou les enzymes cardiaques. En effet, ces derniers possèdent des valeurs prédictives médiocres et ne peuvent être considérés comme outil de triage de ces patients. En revanche, la coronarographie immédiate et systématique (suivie d’une reperfusion coronaire si nécessaire) était associée de manière significative et indépendante à la survie hospitalière (OR ajusté= 2.06 (1.16-3.66)) et ceci quelque soit l’aspect électrocardiographique. Entre 2000 et 2009, 1145 patients ont été admis et 2/3 d’entre eux ont été traités par hypothermie thérapeutique. Parmi eux, 708/1145 (62%) avait initialement un rythme cardiaque choquable et 437/1145 (38%) présentait un rythme non choquable. Après ajustement sur les autres facteurs pronostiques, l’hypothermie thérapeutique avait un rôle protecteur sur le pronostic neurologique des patients à la sortie de réanimation dans le groupe présentant initialement un rythme choquable (OR ajusté= 1.90 (1.18-3.06)). En revanche, l’association entre le pronostic et l’intervention dans le groupe « non-choquable » n’était pas significative (OR ajusté=0.71 (0.37-1.36)). Parmi les facteurs susceptibles d’altérer le bénéfice lié à ce traitement, les complications infectieuses chez les patients traités par hypothermie thérapeutique s’avèrent courantes La plus fréquente est la pneumopathie précoce, dont l’apparition est associée de manière significative au traitement par hypothermie (OR ajusté= 1.90 (1.28-2.80)), mais son rôle sur le pronostic n’est pas démontré
Background: Out-of-Hospital Cardiac Arrest (OHCA), usually clinically described as “sudden death”, is the leading worldwide cause of death. Despite recent improvements in management of OHCA, the prognosis of these patients remains very poor, even in those who benefitted from a successful initial resuscitation. During the period of ischemia following the Return of Spontaneous Circulation (ROSC), several pathophysiological phenomenons occur, characterizing the post cardiac arrest syndrome. Furthermore, different treatments, such as immediate coronary reperfusion or therapeutic hypothermia, are now implemented for the management of this syndrome in order to decrease the morbidities and the mortality involved during this period. However, the influence of these hospital interventions on prognosis is still debatable, since they have been assessed in very selected subgroups of patients.Objectives: The aim of our work was to assess the influence of these early interventions on the outcome of OHCA patients admitted alive in intensive care unit (ICU).Method: We set up an investigation cohort (starting in 2000) of OHCA patients, in whom a successful ROSC had been obtained and who were admitted alive in ICU. We gathered all demographic data, cardiac arrest circumstances, pre-hospital and hospital characteristics. We analyzed the different predictive factors of outcome using multivariate analysis, especially logistical regression.Results: Between 2003 and 2008, 435 patients without obvious extra-cardiac cause were included and benefited from an immediate and systematical coronary angiogram. We observed a recent lesion in nearly half of them. Detecting a cardiac etiology is very challenging even using simple predictive models including patient’s baseline characteristics and circumstances of the cardiac arrest. Moreover, other parameters, such as EKG patterns or cardiac biomarkers, did not seem helpful either. Indeed, these parameters had poor predictive values and consequently could not be considered as triage tools for these patients. Nevertheless, the immediate and systematical coronary angiogram, with percutaneous intervention if appropriate, was independently associated with an improvement of hospital survival (adjusted OR= 2.06 (1.16-3.66)), regardless of the EKG pattern.Between 2000 and 2009, 1145 patients were admitted and two third of them were treated with therapeutic hypothermia. Among them, 708/1145 (62%) had an initial shockable rhythm and 437/1145 (38%) presented a non shockable rhythm. On the one hand, after adjustment with other predictive factors, the therapeutic hypothermia significantly improved the good neurological outcome at ICU discharge (adjusted OR= 1.90 (1.18-3.06)). On the other hand, the influence of this intervention was not associated with prognosis on the “non-shockable” sub-group (adjusted OR=0.71 (0.37-1.36)). Among the undercurrent factors, which could minimize the benefit of this intervention, infectious complications in treated patients were common. The most frequent complication was early onset pneumonia, whose occurrence was significantly associated with hypothermia (adjusted OR= 1.90 (1.28-2.80)), even if its role on prognosis was not determined.Conclusions: Our findings support the international guidelines regarding the management of post-cardiac arrest, identifying the subgroups of patients who may benefit the most. These results encourage further prospective studies and randomized trials and bring helpful information in that way. Finally, ancillary analysis on an investigation cohort of hospital survivors suggests that protective

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Cardin-Ouellette, Sabrina. « La convergence du flux de vapeur d'eau et son potentiel comme variable hydrologique de surface ». Mémoire, École de technologie supérieure, 2013. http://espace.etsmtl.ca/1250/1/CARDIN%2DOUELLETTE_Sabrina.pdf.

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L’hydrologie s’est longtemps intéressée uniquement à la branche terrestre du cycle hydrologique. Pourtant, le contenu en vapeur d’eau de l’atmosphère au-dessus du bassin versant peut varier en fonction du transport net de vapeur d’eau par l’atmosphère soit la convergence horizontale du flux de vapeur d’eau (C). Pour de longues périodes de temps et à l’échelle du bassin, C devrait être égale au ruissellement (R) sortant de cette même région. La convergence du flux de vapeur d’eau pourrait constituer une information supplémentaire d’intérêt afin d’améliorer les modèles hydrologiques visant la prévision du débit en rivière. L’objectif général de ce mémoire est d’évaluer quantitativement le cycle hydrologique complet à l’intérieur du modèle régional canadien de climat (MRCC) afin de déterminer le potentiel de la convergence de flux de vapeur d’eau comme variable utilisable en hydrologie appliquée. Le MRCC est un outil d’intérêt en hydrologie puisqu’il permet de modéliser plusieurs processus complexes du cycle hydrologique à l’échelle régionale, en plus de calculer plusieurs composantes du cycle qui sont difficiles à mesurer dans le monde réel. Les résultats indiquent que la convergence du flux de vapeur d’eau est égale au ruissellement à l’échelle temporelle climatique. À l’échelle annuelle, la convergence et le ruissellement demeurent fortement corrélés (r > 0,8). À l’échelle mensuelle et journalière, la corrélation entre les termes diminue vu l’importance de l’eau transitant dans les réservoirs atmosphérique et terrestres. En hiver, la convergence mensuelle des bassins nordiques est approximativement égale à la variation du couvert de neige. Le terme d’erreur du bilan hydrique représente 0 à 10% de C à l’échelle temporelle climatique. Cet ordre d’erreur est nettement inférieur aux termes d’erreur obtenus par des études similaires faites à partir de réanalyses et ce pour des bassins de plus petites superficies. L’erreur dans le bilan hydrique est liée au schéma numérique semi-lagrangien du MRCC et aux interpolations nécessaires au calcul de C. Pourtant cette erreur supposée aléatoire ne diminue pas strictement avec l’augmentation de la superficie du bassin. Ce biais positif,C < R, pourrait être un biais régional engendré par la correction du bilan hydrique intégré à l’intérieur du MRCC. L’augmentation du terme d’erreur aux échelles mensuelles (0 à 30%) et journalières (0 à plus de 100%) est due à un décalage temporel de 6h entre les flux et les variables d’état lors de leur enregistrement par le MRCC.

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Burford, Evans J. « Myocyte Derived Cardiac Spheroids for Post Infarct Cardiac Regeneration ». Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-theses/145.

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Research has shown that autologous progenitor-like cardiac spheroids, when delivered to an infarcted heart, are able to restore mechanical function. These spheroids are made by isolating and expanding autologous cardiac progenitor cells. Though these results are promising, the process for creating cardiac spheroids is inefficient and time consuming, requiring a large amount of cardiac tissue. For every 10,000 cardiac myocytes in the heart there is only one cardiac progenitor cell; requiring a large amount of initial tissue. This clinical limitation could be overcome if cardiac myocytes, which are more abundant than cardiac progenitor cells, could be used to make cardiac spheroids. Research has shown that mesenchymal stem cells when co-cultured with adult cardiac myocytes cause the cardiac myocytes to behave like a progenitor cell. We found that, when co-cultured with mesenchymal stem cells, cardiac mycoytes could be made to form cardiac spheroid bodies. This was done by isolating adult myocytes from rat hearts and co-culturing them with human mesenchymal stem cells. After two weeks, cultures were observed to form spheroid bodies and the number of spheroids formed were compared to a pure myocyte control. Cardiac specific staining confirmed that the spheroids were made from the myocytes. It was also found that the mesenchymal stem cells, when co-cultured in the same well with the myocytes, form significantly more spheroids than myocytes treated with stem cell conditioned media. Further, no other cell type present in the co-cultures are able to create spheroid bodies when co-cultured with mycoytes or stem cells. The ability to create cardiac spheroid like bodies from adult myocytes offers a way to overcome the limitations of the time needed and the large quantity of autologous cardiac tissue required to currently make these types of bodies.

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Stirparo, G. G. « DEFINITION OF TRANSCRIPTIONAL LANDSCAPE IN CARDIAC MATURATION AND CARDIAC HYPERTROPHY ». Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/247064.

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Heart failure (HF) is a syndrome resulting from a complex genetic predisposition and multiple environmental factors: it is a leading cause of morbidity and mortality. Specific gene expression patterns are activated in the hypertrophic and failing heart and are thought to contribute to the development of HF. Many regulatory molecules are involved in the control of gene expression: among these, long non-coding RNA (lncRNA) is gaining importance for several cellular process and diseases. However, little is still known about its involvement in HF. Many functions have been attributed to lncRNAs, such as cell proliferation, apoptosis and cell invasion, indicating that they may represent a major regulatory component of the eukaryotic genome. Not surprisingly, lncRNAs have been found implicated in several aspects of cancer, and in many neuronal diseases. Despite this, and the known role of other ncRNAs, such as miRNA, in HF, the function of lncRNAs in this pathologic state has been not studied. Thus, the general hypothesis behind this project is that lncRNAs have an important role in defining gene expression re-programming in HF. Consequently, the overall scientific objective of this proposal is to study the role of lncRNAs in gene transcription regulation accompanying heart failure. To this end, we propose to use high-throughput RNA sequencing (RNA-seq) to identify lncRNAs that are modulated in cardiomyocytes during HF. In order do to this, we performed RNA-seq on cardiomyocytes isolated from mice after 1, 2, 4 and 7 days of transverse aortic constriction (TAC) and from sham-operated mice. The importance of this study lies not only in the furthering of our understanding of the pathological mechanisms leading HF, but aims to generate – in the light of recent progress in RNA-based therapeutic strategies – data that may be instrumental to the development of improved therapeutic strategies for this increasingly frequent pathology.

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Dawson, Jennifer Elizabeth. « Cardiac Tissue Engineering ». Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20071.

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The limited treatment options available for heart disease patients has lead to increased interest in the development of embryonic stem cell (ESC) therapies to replace heart muscle. The challenges of developing usable ESC therapeutic strategies are associated with the limited ability to obtain a pure, defined population of differentiated cardiomyocytes, and the design of in vivo cell delivery platforms to minimize cardiomyocyte loss. These challenges were addressed in Chapter 2 by designing a cardiomyocyte selectable progenitor cell line that permitted evaluation of a collagen-based scaffold for its ability to sustain stem cell-derived cardiomyocyte function (“A P19 Cardiac Cell Line as a Model for Evaluating Cardiac Tissue Engineering Biomaterials”). P19 cells enriched for cardiomyocytes were viable on a transglutaminase cross-linked collagen scaffold, and maintained their cardiomyocyte contractile phenotype in vitro while growing on the scaffold. The potential for a novel cell-surface marker to purify cardiomyocytes within ESC cultures was evaluated in Chapter 3, “Dihydropyridine Receptor (DHP-R) Surface Marker Enrichment of ES-derived Cardiomyocytes”. DHP-R is demonstrated to be upregulated at the protein and RNA transcript level during cardiomyogenesis. DHP-R positive mouse ES cells were fluorescent activated cell sorted, and the DHP-R positive cultured cells were enriched for cardiomyocytes compared to the DHP-R negative population. Finally, in Chapter 4, mouse ESCs were characterized while growing on a clinically approved collagen I/III-based scaffold modified with the RGD integrin-binding motif, (“Collagen (+RGD and –RGD) scaffolds support cardiomyogenesis after aggregation of mouse embryonic stem cells”). The collagen I/III RGD+ and RGD- scaffolds sustained ESC-derived cardiomyocyte growth and function. Notably, no significant differences in cell survival, cardiac phenotype, and cardiomyocyte function were detected with the addition of the RGD domain to the collagen scaffold. Thus, in summary, these three studies have resulted in the identification of a potential cell surface marker for ESC-derived cardiomyocyte purification, and prove that collagen-based scaffolds can sustain ES-cardiomyocyte growth and function. This has set the framework for further studies that will move the field closer to obtaining a safe and effective delivery strategy for transplanting ESCs onto human hearts.

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Peace, Richard Aidan. « Quantitative cardiac SPECT ». Thesis, University of Aberdeen, 2001. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602292.

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Myocardial perfusion SPECT imaging is a sensitive and specific indicator of coronary artery disease (Fleischman et al. 1998). The clinical value of coronary scintigraphy is now established with a utilisation rate of eight procedures per 1000 population per year in the USA and two per 1000 in the EU (Pennell et al. 1998). While myocardial perfusion SPECT images are routinely interpreted by expert observers the classification is inevitably subject to inter-observer and intra-observer variability. An optimised and validated quantitative index of the presence or absence of coronary artery disease (CAD) could improve reproducibility, accuracy and diagnostic confidence. There are segmental techniques to automatically detect CAD from myocardial perfusion SPECT studies such as the CEqual quantitative analysis software (Van Train et al. 1994). However, they have not been shown to be significantly better than expert observers (Berman et al. 1998). The overall aim of this thesis was to develop, optimise and evaluate quantitative techniques for the detection of CAD in myocardial perfusion SPECT studies. This task was divided into three areas; quantification of transient ischaemic dilation (TID); quantitative detection and localisation of CAD; count normalisation of patient studies. Transient ischaemic dilation (TED) is the transient dilation of the left ventricle on immediate post stress images compared to resting technetium-99m imaging. Stolzenberg (1980) first noted TID as a specific marker for severe CAD. There are few published studies of fully quantitative evaluations of TID. The first aim of this thesis was to compare the performance of methods for quantifying TDD in myocardial perfusion SPECT. The second aim of this thesis was to investigate the use of image registration in myocardial perfusion SPECT for quantitative detection and localisation of CAD. This thesis describes two studies comparing six count normalisation techniques. These techniques were; normalise to the maximum value; to the mean voxel value; to the mean of the top 10% or 20% of counts; minimise the sum of squares between studies or the sum of absolute differences. Ten normal myocardial perfusion SPECT studies each with 300 different simulated perfusion defects were count normalised to the original studies. The fractional count normalisation error was consistently lower when the sum of absolute differences was minimised. However, a more clinically applicable measure of count normalisation performance is the effect on quantitative CAD detection. The Z-score method of automatic detection of CAD was repeated using each count normalisation technique. There was no statistically significant difference between the methods although the power of the ROC analysis was poor due to low patient numbers. The balance of evidence suggested that count normalisation by minimisation of the of absolute differences produced the best performance.

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Semenas, Egidijus. « Sex Differences in Cardiac and Cerebral Damage after Hypovolemic Cardiac Arrest ». Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-146314.

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Resuscitation from haemorrhagic shock and the subsequent circulatory arrest remains a major clinical challenge in the care of trauma patients. Numerous experimental studies in sexually mature animals have shown a gender dimorphism in response to trauma and haemorrhagic shock. The first study was designed to evaluate sex differences in outcome after resuscitation from hypovolemic circulatory arrest. We intended to examine innate sex differences, and chose to study sexually immature animals. The study showed that cerebral cortical blood flow was greater, blood-brain-barrier was better preserved and neuronal injury was smaller in female as compared to male piglets. The second study demonstrated that female sex was associated with enhanced haemodynamic response, cardioprotection, and better survival. This cardioprotective effect was observed despite comparable estradiol and testosterone levels in male and female animals, indicating an innate gender-related cardioprotection. In both studies (I and II) female sex was associated with a smaller increase in the cerebral expression of inducible and neuronal nitric oxide synthase (iNOS and nNOS). Thus in the study III we tested the hypothesis that exogenously administered 17β-estradiol (E2) could improve neurological outcome by NOS modulation. The results showed that compared with the control group, animals in the E2 group exhibited a significantly smaller increase in nNOS and iNOS expression, a smaller blood-brain-barrier disruption and a mitigated neuronal injury. There was also a significant correlation between nNOS and iNOS levels and neuronal injury. A hypothesis if female-specific cardioprotection may be attributed to a smaller NOS activity was tested in study IV. The animals received methylene blue (MB) during CPR, but were otherwise treated according to the same protocol as studies I-II. The female-specific cardioprotection could be attributed to a smaller NOS activity, but NOS inhibition with MB did not improve survival or myocardial injury, although it abated the difference between the sexes.

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Ede, Mauricio. « An alternative agent to induce cardiac arrest for normothermic cardiac surgery ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0022/NQ32879.pdf.

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Thomas, Nia Lowri. « Molecular mechanisms underlying cardiac ryanodine receptor dysfunction in sudden cardiac death ». Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/54084/.

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Ca²⁺ release via the cardiac ryanodine receptor (RyR2) is a fundamental event in excitation-contraction coupling. Point mutations in the gene encoding RyR2 are associated with arrhythmogenic right ventricular dysplasia type 2 (ARVD2), a disease likely characterised by abnormal release of Ca²⁺ that may result in sudden death. GFP-tagged RyR2 mutants (R¹⁷⁶Q/T²⁵⁰⁴M, L⁴³³P and N²³⁸⁶I) were generated and expressed in a human embryonic kidney (HEK) cell model, enabling profiling of the amplitude and temporal characteristics of caffeine-evoked Ca²⁺release through homotetrameric channels using confocal microscopy. Mutants were functionally heterogeneous and demonstrated profound differences in Ca²⁺ release when compared with WT channels, including the novel observation that one of the mutants (L⁴³³P) exhibited reduced sensitivity to caffeine activation. The molecular basis of this heterogeneity was investigated by determining the sensitivity of the mutant channels to cytoplasmic Ca²⁺. This was achieved by evaluation of caffeine-induced Ca²⁺ release from WT or mutants channels in streptolysin-O permeabilised HEK cells, where the cytoplasmic Ca²⁺ concentration was clamped. Although resting ER Ca²⁺store and cytoplasmic Ca²⁺ levels were comparable in all cells, RyR2 mutants were characterised by a profound loss of Ca²⁺-dependent inactivation. We also investigated whether these mutations disrupted the interaction between RyR2 and accessory proteins involved in normal channel function. cDNA encoding mutation susceptible regions were constructed and screened against a human cardiac cDNA library using a yeast two hybrid system. The N²³⁸⁶I mutation abolished association of the RyR2 domain with two cardiac proteins, which robustly occurred with the corresponding WT domain. These findings demonstrate that ARVD2-linked RyR2 mutations critically affect channel activation and suggest that differential sensitivity to cytoplasmic Ca²⁺ may be a causative mechanism in the pathogenesis of this disease.

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Drexler, Samona Smith. « Quality Improvement Project| Cardiac Risk Stratification Prior to Non-Cardiac Surgery ». Thesis, University of Louisiana at Lafayette, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10163292.

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The occurrence of major adverse cardiac events (MACE) is a common perioperative complication and contributing factor for the increase risk of morbidity and mortality in adult patients undergoing non-cardiac surgery. The most reasonable and evidence-based option to reduce the risk of MACE and perioperative morbidity and mortality is a consistent assessment of the functional capacity for non-cardiac patients prior to non-cardiac surgical procedures. According to Fleisher et al. (2014), individuals with a decreased or unmeasurable functional capacity should be referred to a cardiologist for evaluation and cardiac risk stratification prior to surgery. The Duke Activity Status Index (DASI) tool has demonstrated to be an effective tool in assessing functional capacity and identifying individuals without a known cardiac history who may be at risk for perioperative cardiac complications.

This quality improvement project focused on the implementation and use of the DASI tool into the preexisting formal preoperative procedure. Use of the DASI tool focused on accurate measurements of the surgical patient’s functional capacity and evaluation of potential risk factors for MACE. As a result of using the DASI tool in the preoperative process, several non-cardiac adult patients were recognized as being at risk for MACE and underwent cardiac interventional procedures following referral to a cardiologist for preoperative evaluation. Assessing functional capacity using the DASI tool prior to non-cardiac surgical procedures has proven to be both valuable and medically beneficial for the non-cardiac adult patients in evaluation of the risk for MACE.

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Johnson, Jonas. « The Cardiac State Diagram : A new method for assessing cardiac mechanics ». Doctoral thesis, KTH, Medicinsk avbildning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-202743.

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Jeffords, Megan E. « Tailoring Material Properties Of Cardiac Matrix Hydrogels For Cardiac Tissue Engineering ». University of Akron / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=akron1430838968.

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Yamada, Tetsu. « Impact of the cardiac arrest mode on cardiac death donor lungs ». Kyoto University, 2015. http://hdl.handle.net/2433/200492.

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Nicholson, Suzanne Maria. « Uncertainty in cardiac transplant recipients prior to and after cardiac catheterization ». Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276609.

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The purpose of this study was to describe the presence of uncertainty experienced by heart transplant recipients at one and two year diagnostic follow-up evaluations. Twelve one year and eleven two year transplant recipients completed the Mishel Uncertainty in Illness Scale (MUIS), prior to and after cardiac catheterization. There was a decrease in uncertainty levels from pre to post-catheterization, for both one and two year recipients, however, findings were not significant. Recipients prior experience with catheterization and the interaction effects of the complete evaluation process or future health status may have affected the subject's uncertainty response. Two year transplant recipients demonstrated significantly higher uncertaintly levels, before and after cardiac catheterization, when compared to one year recipients. These findings lend initial and tentative support to the proposal that uncertainty increases with time post-transplant. The yearly follow-up evaluation may represent an episodic focusing for the transplant recipient on health status.

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Gibbons, David D. « Stabilization of the Cardiac Nervous System During Cardiac Stress Induces Cardioprotection ». Digital Commons @ East Tennessee State University, 2012. https://dc.etsu.edu/etd/1219.

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The cardiac nervous system consists of nested reflex feedback loops that interact to regulate regional heart function. Cardiac disease affects multiple components of the cardiac nervous system and the myocytes themselves. This study aims to determine: 1) how select components of the cardiac nervous system respond to acute cardiac stress, including myocardial ischemia (MI) and induced neural imbalance leading to cardiac electrical instability, and 2) how neuromodulation can affect neural-myocyte interactions to induce cardioprotection. Thoracic spinal cord stimulation (SCS) is recognized for its anti-anginal effects and ability to reduce apoptosis in response to acute MI, primarily via modulation of adrenergic efferent systems. The data presented here suggest that cervical SCS exerts similar cardioprotective effects in response to MI, but in contradistinction to thoracic SCS, uses both adrenergic and cholinergic efferent mechanisms to stabilize cardiomyocytes and the arrhythmogenic potential. SCS potentially can use efferent and/or anti-dromically activated cardiac afferents to mediate its cardioprotection. Thoracic SCS mitigates the MI-induced activation of both nodose and dorsal root ganglia cardiac-related afferents, doing so without antidromic activation of the primary cardiac afferents. Instead, thoracic SCS acts through altering the cardiac milieu thereby secondarily affecting the primary afferent sensory transduction. In response to cardiac stressors, reflex activation of efferent activity modifies mechanical and electrical functions of the heart. Excessive activation of neuronal input to the cardiac nervous system can induce arrhythmias. Stimulation of intrathoracic mediastinal nerves directly activates subpopulations of intrinsic cardiac neurons, thereby inducing atrial arrhythmias. Neuromodulation, either thoracic SCS or hexamethonium, suppressed mediastinal nerve stimulation (MSNS)-induced activation of intrinsic cardiac neurons and correspondingly reduced the arrhythmogenic potential. SCS exerted its stabilizing effects on neural processing and subsequent effects on atrial electrical function by selectively targeting local circuit neurons within the intrinsic cardiac nervous system. Together these data indicate that neuromodulation therapy, using SCS, can mitigate the imbalances in cardiac reflex control arising from acute cardiac stress and thereby has the potential to slow the progression of chronic heart disease.

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Belian, Elisa. « The instructive role of cardiac transcription factors in triggering transition of cardiac progenitor cells into the cardiac muscle fate ». Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/40196.

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The mechanisms that maintain cardiac progenitor cells (CPCs) in a state of arrested development and prevent their spontaneous differentiation are unknown. This study is aimed at investigating potential mechanisms responsible for the striking paradox of cardiac transcription factors' expression without activation of their direct cardiomyocyte-specific target genes. Expression analysis of a range of CPC-derived clonal lines, characterised by Sca-1 expression and the SP phenotype, showed that all analysed cardiac transcription factors are expressed as nuclear-localised proteins. Hence, the absence of nucleartargeted protein expression is not the reason for lack of transcriptional activity. Interestingly, none of the clones expressed the complete triad of Gata4, Mef2c and Tbx5 (GMT) that reportedly reprograms cardiac fibroblasts into cardiomyocytes. However, forced expression of the respective missing factor(s) in CPCs induced few of the tested cardiac markers, indicating that lack of co-expression of these three factors is not the reason for the cells' failure to undergo differentiation. As a third potential barrier, the cardiac muscle-specific isoform of the transcriptional coactivator Myocardin (Myocd) was investigated and found to be absent in all analysed clones. Conversely, rescue with exogenous Myocd plus Tbx5 was found to robustly activate nearly all tested RNA and protein markers diagnostic of the cardiomyocyte lineage. In summary, this study demonstrates that rescuing the lack of Myocd in combination with other cardiac transcription factors is sufficient to induce expression of a range of cardiac genes and proteins characteristic of differentiated cardiomyocytes, suggesting that the lack or insufficient level of these factors is a limiting mechanism maintaining CPCs in the undifferentiated state. Evidence presented in this study indicates that Myocd is not only crucial in regulating cardiac muscle formation during embryogenesis but pivotal to induce the transition of adult cardiac progenitor cells toward the cardiac muscle fate.

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Carlan, Eliana. « Sistemas de Organização do Conhecimento : uma reflexão no contexto da Ciência da Informação ». Thesis, reponame:Repositório Institucional da UnB, 2010. http://eprints.rclis.org/14519/1/Carlan-Eliana-Dissertacao.pdf.

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This research studies the knowledge organization systems (KOS) related to theories to build thesaurus, taxonomies, ontologies and classification systems in the literature field of Information Science. It uses the methodology of literature review and a research on the same field databases in order to investigate the bibliographic production about the theme, from 1998 up to July 2009. A bibliographic research about knowledge organization and representation is carried out, specifically related to the development of thesaurus, taxonomies, ontologies and classification systems. It identifies the same theoretical way to build KOS through the classification theory, concept theory, the relationship between the concepts and the foundation of Linguistics and Terminology. Extrinsic and intrinsic characteristics were analysed from the representative sample of the bibliographic production about KOS. The extrinsic analysis is relative to form aspects, including the publication year, authors, title, publication and keywords. The intrinsic analysis relates to content aspects through the subject analysis of the documents following the theoretical foundations. The last chapter verifies that the thesaurus and classification systems are the most quoted in the literature about KOS, being a theoretical reference to the development of these systems based on the international standards and rules. It highlights the importance of consolidating common standards to build different types of KOS in the field of Information Science and shows the need of gathering the multidisciplinary interests linked by the same goals and also getting better practices in the knowledge organization and representation.

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Mayfield, Audrey. « Encapsulation of Cardiac Stem Cells to Enhance Cell Retention and Cardiac Repair ». Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31500.

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Despite advances in treatment, heart failure remains one of the top killers in Canada. This recognition motivates a new research focus to harness the fundamental repair properties of the human heart, with human cardiac stem cells (CSCs) emerging as a promising cell candidate to regenerate damaged myocardium. The rationale of this approach is simple with ex vivo amplification of CSCs from clinical grade biopsies, followed by delivery to areas of injury, where they engraft and regenerate the heart. Currently, outcomes are limited by modest engraftment and poor long-term survival of the injected CSCs due to on-going cell loss during transplantation. As such, we explored the effect of cell encapsulation to increase CSC engraftment and survival after myocardial injection. Transcript and protein profiling of human atrial appendage sourced CSCs revealed strong expression the pro-survival integrin dimers αVβ3 and α5β1- thus rationalizing the integration of fibronectin and fibrinogen into a supportive intra-capsular matrix. Encapsulation maintained CSC viability and expression of pro-survival transcripts when compared to standard suspended CSCs. Media conditioned by encapsulated CSCs demonstrated superior production of pro-angiogenic/ cardioprotective cytokines, angiogenesis and recruitment of circulating angiogenic cells. Intra-myocardial injection of encapsulated CSCs after experimental myocardial infarction favorably affected long-term retention of CSCs, reduced scar burden and improved overall cardiac function. Taken together, cell encapsulation of CSCs prevents detachment induced cell death while boosting the mechanical retention of CSCs to enhance repair of damaged myocardium.

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Yılmaz, Ayten. « Studies on cardiac pacing emphasis on pacemaker sensors and cardiac resynchronization therapy / ». [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/79548.

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Williams, Lynne Kirsty. « Mechanisms by which cardiac resynchronisation therapy improves cardiac performance in heart failure ». Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/1051/.

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This thesis assesses the mechanisms by which biventricular and left ventricular pacing improves cardiac performance in patients with heart failure. We demonstrated for the first time that CRT results in an improvement in acute haemodynamic variables in heart failure patients with a narrow QRS duration that is comparable to the effects seen in heart failure patients with a broad QRS duration. In addition, we have shown that both biventricular (BIVP) and left ventricular pacing (LVP) significantly reduce external constraint to left ventricular filling, resulting in an increase in effective filling pressure. In heart failure patients with evidence of external constraint at rest, the acute haemodynamic benefits of both BIVP and LVP were principally due to the relief of external constraint and preload recruitment. However, in those patients with evidence of electrical dyssynchrony and a broad QRS duration, a significant haemodynamic benefit was derived from an enhancement in left ventricular contractility, presumably as a result of a reduction in left ventricular dyssynchrony. Patients with external constraint appear to derive a greater haemodynamic benefit from pacing due to the significant increase in stroke work that is associated with relief of external constraint and preload recruitment, in addition to the increase in stroke work derived from enhanced contractility due to a reduction in dyssynchrony. These findings will inform better patient selection for this therapy and also optimisation of pacing strategy in individual patients.

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Mendoza, James Patrick. « The cardiac myocyte-specific role of PKG-1 alpha in cardiac remodeling ». Thesis, Boston University, 2012. https://hdl.handle.net/2144/12517.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Current dogma holds that the cGMP dependent protein kinase (PKG) acts in the cardiovascular system (CVS) mainly through the vascular smooth muscle cell (VSMC) to regulate blood flow and vascular tone via nitric oxide (NO) induced vasodilation. Yet, the role of PKG in the CVS, outside the VSMC, remains largely unexplored. Recent studies have revealed that PKG also functions as an anti-hypertrophic molecule in the heart, attenuating cardiac remodeling and preventing the progression of congestive heart failure (CHF). However, those studies used pharmacological agents which increased whole-body cGMP to activate PKG. One more attractive therapeutic strategy would be to activate PKG in cell-types specific to the heart, but not to the peripheral vasculature, since this might provide a more direct treatment for CHF with fewer adverse side effects. Therefore, we tested the specific hypothesis that PKG-Iα attenuates cardiac hypertrophy and remodeling in vivo through a specific role inthe cardiac myocyte (CM). Genotypically, we compared aMHC-Cre+/-, PKG-Iαfl/fl (Cre+) mice to aMHC-Cre-/-, PKG-Iαfl/fl (Cre-) control mice. Here we have shown that Cre+ mice lose the ability to inhibit cardiac remodeling in an unstressed state. Cre+ mice have increased heart weights, CM size, fibrosis, and contractile dysfunction, compared to Cre- mice. Additionally, Cre+ mice show increased fetal gene expression indicative of remodeling. Lastly, these effects worsened in an age-dependent manner. These data suggest that inhibition of cardiac remodeling occurs principally through PKG-Iα in the CM, and reveal new roles for PKG in the CVS, and as a novel target for CHF therapy.

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Fan, Zhaobo. « Control of Cardiac Extracellular Matrix Degradation and Cardiac Fibrosis after Myocardial Infarction ». The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1480662216531284.

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Whelen, Elizabeth Anne. « Illness perceptions, cardiac rehabilitation and quality of life in cardiac surgery patients ». Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/illness-perceptions-cardiac-rehabilitation-and-quality-of-life-in-cardiac-surgery-patients(63ce3eb5-16c7-487a-8d51-c727a4399a19).html.

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Background: Previous research indicates that for some individuals, quality of life (QoL) post-cardiac surgery (CABG or PTCA ) declines from pre-surgery levels. Using the framework of Leventhal's Common-Sense Model, this longitudinal study examined the associations between patients' illness perceptions and coping strategies, their QoL, attendance at cardiac rehabilitation and lifestyle changes. It was hypothesised that a more negative profile of illness beliefs (weaker control beliefs, belief in more severe consequences, poorer understanding of the condition, and negative emotional representations) together with the use of more emotional coping strategies would be associated with poorer QoL. It was also hypothesised that attendance at cardiac rehabilitation would be associated with greater control beliefs, more severe consequences and a causal attribution of lifestyle. Sample and Methods: 113 patients (93 male, mean age 66 (8.93) who were about to undergo cardiac surgery were recruited from two hospitals. Questionnaire measures of illness perceptions (IPQ-R), coping (CHIP) and cardiac-specific QoL (MacNew) were administered at four time points: pre-surgery, post-surgery, post cardiac rehabilitation, and one-year follow up. Data on attendance at rehabilitation and health behaviours were collected via hospital records and patient report. Results: The best predictors of QoL were not cognitive representations of the cardiac problems, but negative emotional representations and associated emotion-focussed coping strategies, implying that an emotion-regulation intervention could be targeted to improve outcome. The predictive ability of initial QoL on QoL at later stages implies this might be best introduced pre-surgery. Having less severe consequence beliefs prior to surgery predicted greater attendance at cardiac rehabilitation. A better understanding of the cardiac condition predicted attendance at cardiac rehabilitation. There was no evidence of change in lifestyle post-rehabilitation.Discussion: The findings that emotional representations of cardiac problems and the use of emotion focussed coping strategies were predictors of quality of life suggest that interventions to foster adaptive emotion regulation may improve outcome in these patients. Findings with respect to attendance at rehabilitation varied somewhat from the previous literature, possibly because the present study sampled patients who were having elective surgery, rather than those who had recently had a heart attack. The importance of studying defined populations and also the issue of when measures are obtained in relation to cardiac events were also highlighted.

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Lionetti, Fred. « GPU accelerated cardiac electrophysiology ». Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p1474756.

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Thesis (M.S.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed April 14, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 85-89).

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De, Vos Jacques Pinard. « Automated pediatric cardiac auscultation ». Thesis, Link to the online version, 2005. http://hdl.handle.net/10019/1008.

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Lord, Stephen. « Reinnervation after cardiac transplantation ». Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410568.

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Bach, Thuthuy. « Computerized cardiac mapping system ». Thesis, University of Ottawa (Canada), 1990. http://hdl.handle.net/10393/5878.

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This thesis presents the results of the work on a computerized cardiac mapping system for recording simultaneously the signals from three electrodes placed at different sites on the heart in order to diagnose the sites causing arrhythmias. The signals are buffered, amplified, filtered and transferred to a personal computer via a multiplexing A/D converter. The computer controls the data acquisition process and stores the data in the memory. Activation times of the heart are estimated by a computer algorithm and displayed on a screen. The digitized waveforms and the vertical time marker of the activation time on each waveform are also displayed for verification. Corrections of computer-estimated activation times are possible using an interactive computer program. With this system, the region initiating an arrhythmia can be localized within a few minutes. The system has been used clinically and proved to be effective in detection of the sites of early activation causing cardiac arrhythmia.

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Lodgek, Erika. « History of Cardiac Anesthesia ». The University of Arizona, 2018. http://hdl.handle.net/10150/626588.

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Lipšic, Erik. « Erythropoietin in cardiac ischemia ». [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/293076030.

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Robinson, Monique Renee. « Cardiac pathophysiology of obesity ». Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414224.

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Kluvitse, C. D. « Discrimination of cardiac activity ». Thesis, University of Hull, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233949.

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43

Al-raqad, Mohammed. « Cardiac involvement in dystrophinopathies ». Thesis, University of Newcastle Upon Tyne, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627742.

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Taylor, Kelly A. « Benefits of cardiac rehabilitation ». Honors in the Major Thesis, University of Central Florida, 2001. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/251.

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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.
Bachelors
Health and Public Affairs
Nursing

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45

Smetana, Peter. « Dynamics of cardiac repolarisation ». Thesis, St George's, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479379.

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46

Bourke, L. T. « Cardiac injury in lupus ». Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1458423/.

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Systemic lupus erythematosus (SLE) carries a significantly enhanced risk of developing cardiovascular disease (CVD) and remains a leading cause of death in these patients, accounting for ~25% of all causes of mortality. Although there is clear evidence li nking accelerated atherosclerosis to SLE (and consequently an increase in cardiovascular events), another factor that may contribute to CVD related morbidity and mortality is reperfusion injury that occurs post - ischaemia. This is termed ischaemic / reperfu sion (I/R) injury and is a known important contributor to the size of the eventual infarct in the heart, which in animal studies has been shown to account for up to 40 - 50% of the final infarct size. Hydroxychloroquine (HCQ), originally an anti - malarial dr ug, is now used to treat autoimmune disorders, including SLE. HCQ has been shown to modulate inflammation in rheumatic diseases such as SLE and rheumatoid arthritis as well as have potential cardiovascular benefits in these patients. One of the keys aims o f this thesis was to explore the potential use of HCQ in reducing cardiac I/R injury. HCQ was found to be cardioprotective in an in vitro neonatal cardiomyocytes simulated I/R injury model as well as in an in vivo cardiac I/R injury model. This was found to be through an ERK - dependent mechanism which was blocked in the presence of the ERK inhibitor U0126 both in vitro and in vivo . Another relevant question addressed in this thesis was if I/R injury is enhanced in lupus. There is evidence from an autoimmune prone mouse model that lupus IgG are pathogenic in mesenteric I/R injury . However, no study as yet has investigated human lupus IgG in a heart model. IgG was purified from the serum of SLE patients (aPL +ve vs aP L – ve), antiphospholipid syndrome (APS) patients, juvenile onset SLE (JSLE) patients and healthy volunteers. The pre - treatment of neonatal rat cardiomyocytes with IgG from all 3 patient groups enhanced simulated I/R injury. However, the most pathogenic wer e those who were aPL positive. Interestingly, JSLE patients who were all aPL negative, enhanced I/R injury to similar levels as those who tested positive in the adult patient cohort. An enhanced p38 MAPK phosphorylation was observed in the presence of aPL positive IgG and this pathogenic effect was blocked in the presence of the p38 inhibitor SB23580. The results ob tained in this thesis have identified a potential role for HCQ in the cardiovascular field as a cardioprotective therapeutic in myocardial I/R injury. Additionally , IgG purified from patients with SLE , APS and JSLE have been shown to accelerate myocardial I/R injury.

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Couper, Keith. « Debriefing for cardiac arrest ». Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/67921/.

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Early data from North America supports the use of educational cardiac arrest debriefing as a strategy to improve the quality of cardiopulmonary resuscitation (CPR) in the hospital setting. As some debriefing approaches are challenging to deliver in the NHS setting, there was a need to develop debriefing approaches that are both effective and suited to NHS working practices. This thesis is modelled on the Medical Research Council framework for the development and evaluation of complex interventions. Undertaken between October 2011 and January 2015, it describes the development and feasibility assessment of three cardiac arrest debriefing approaches, which were specifically designed to be deliverable in NHS hospitals. Development work comprised three work packages (systematic review, process evaluation, qualitative study). These studies provided evidence to support the use of cardiac arrest debriefing, but showed that weekly group debriefing is undeliverable in many NHS hospitals. Through qualitative work, I identified six distinct mechanisms by which debriefing may affect clinical practice. Synthesis of these data led to the development of three cardiac arrest debriefing approaches (monthly group debriefing, individual oral debriefing, written feedback). We tested the feasibility of delivering these interventions by implementing them in three NHS hospitals (one intervention per hospital). In a before/after study, it was demonstrated that, despite practical challenges, interventions were deliverable in NHS hospitals. However, they were found to have no effect on either CPR quality or patient outcome. This finding was attributed to high performance in study hospitals at baseline. This thesis demonstrates that the developed cardiac arrest debriefing interventions are deliverable in NHS hospitals. It has also generated important new theory about the mechanisms by which debriefing may affect clinical practice. This thesis lays the foundation for future work to evaluate the clinical and cost-effectiveness of these cardiac arrest debriefing interventions.

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Cook, Stuart Alexander. « Regulation of cardiac apoptosis ». Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393164.

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Couderc, Jean-Paul. « Le cancer du cardia ». Nantes, 1988. http://www.theses.fr/1988NANT124M.

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Akinjolire, O. J., et J. H. Mohanad. « Open-chest cardiac massage ». Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32745.

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Open-chest cardiac massage is an emergency procedure for managing a heart that is not beating or beating ineffectively(cardiac arrest). It is done in conjunction with the administration of drugs directly into the heart or vein and the use of direct electrical defibrillation. It is applied in chest surgery, chest injuries or n chest rigidity that precludes adequate external massage. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/32745

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Thèses sur le sujet « Cardak »

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