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Loonat, Aminah Ahmed. "The involvement of p38 gamma MAPK in pathological cardiac hypertrophy." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-involvement-of-p38gamma-mapk-in-pathological-cardiac-hypertrophy(f00e26a7-dab2-474d-9d3e-a52dfe9e873e).html.
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p38-mitogen activated protein kinases (p38-MAPKs) are stress activated serine/threonine kinases that are activated during several different cardiac pathologies. Classically, studies have focused solely on p38α signaling in the heart. However, there is also high cardiac expression of the p38γ isoform but little is known about its cardiac function. The aim of this study was to elucidate the signaling pathway of p38γ, with a particular focus on its role in the progression of pathological cardiac hypertrophy. Comparisons of cardiac function and structure of wild type (WT) and p38γ knock out (KO) mice, in response to abdominal aortic banding, found that KO mice developed less ventricular hypertrophy than their corresponding WT controls, and have preserved cardiac function. Basal p38γ myocardial staining was primarily localised at the membranes and throughout the cytoplasm. Following aortic constriction, nuclear staining of p38γ increased, but no accumulation of p38α was observed. This suggests that the two isoforms play distinct roles in the heart. To elucidate its signaling pathway, we generated an analogue sensitive p38γ, which is mutated at a gatekeeper residue, to specifically track and identify its endogenous substrates in the myocardium. The mutation allows only the mutant kinase, but not WT kinases, to utilise analogues of ATP that are expanded at the N6 position and contain a detectable tag on the γ-phosphate. Transfer of this tag to substrates allows subsequent isolation and identification. Furthermore, unlike other p38-MAPKs, p38γ contains a C-terminal PDZ domain interacting motif. We have utilised this motif in co pull-down assays to identify interacting proteins of p38γ in the heart. Using these techniques we have identified, amongst other substrates, LDB3 and calpastatin as novel substrates of p38γ and we have determined the residues that are targeted for phosphorylation. Lastly we have shown that phosphorylation of calpastatin reduces its efficiency as a calpain inhibitor in vitro, hence proposing a mechanism by which p38γ may mediate its pro-hypertrophic role.
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Pell, Theresa Jane. "The involvement of ATP-sensitive potassium channels in novel forms of myocardial protection." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314289.
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Prosser, Hamish Charles Graydon. "Involvement of Novel Cardiac Peptides in Healthy and Ischemic Hearts." Thesis, University of Canterbury. Biological Sciences, 2009. http://hdl.handle.net/10092/2731.
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The role and functions of Urotensin II (UII), Urotensin II-related peptide (URP) and proangiotensin-12 (PA12) are currently ambiguous, either due their relatively new identification and isolation from their host species, or due to contrasting and conflicting reports observing the physiological and pathophysiological role of these spasmogens within the mammalian cardiovascular system. Accordingly, we sought to determine the true physiological functions of these peptides in both healthy and diseased states. The initial task was to reveal potential reasons for the contrasting responses to UII, and to define the role of UII within the isolated rat heart. UII and URP retain a highly conserved cyclic region, shown to be necessary in receptor binding and activation, with the high inter-species variance within the N-terminus reported to be of little importance. Our research revealed UII to be highly species-specific, stimulating potent, sustained vasodilation of the coronary arteries in response to the native form infused, while non-native UII peptides had either no effect, or caused significant vasoconstriction. UII-induced vasodilative effects were found to be mediated by nitric oxide and prostaglandin activity combined. Reviewing publications to date it was evident that many studies employed UII foreign to the host species, reporting potentially untrue effects, based on our findings. Recent studies have identified UII as a potent agent in developing and promoting atherosclerosis and coronary artery disease through UII-induced mitogenic activity and promoting foam cell formation. Hence, we observed the effect of infusing the native species of UII and URP into a model of cardiac ischemia-reperfusion. Both preconditioning the heart with UII or URP, or infusing UII or URP upon reperfusion caused significant coronary vasodilation following ischemia, and significantly attenuated ischemic-induced myocardial injury. These studies indicated elevating UII and URP provided a level of cardioprotection, not only when administered into healthy hearts prior to an ischemic event, but also in hearts having already undergone ischemia and the resultant endothelial damage. PA12 was the third peptide tested in the current thesis. Being newly identified and suggested to be a new component of the renin-angiotensin system (RAS) it was important to define the physiological role of PA12 upon the cardiovasculature, as the RAS is heavily associated with the development and progression of cardiovascular disease. Utilising the Langendorff isolated rat heart technique, PA12 was found to cause potent vasoconstriction of the coronary arteries, mediated by the angiotensin II type 1 receptor (AT₁R). Furthermore, using subjecting the perfusate samples to radioimmunoassay and RP-HPLC revealed PA12 was converted to AngII. Both PA12-induced vasoconstriction and generation of AngII were found to be dependent upon chymase activity, with inhibition of ACE1 having little effect. Myography was employed to further study the vascular response to PA12 throughout the rat arterial system from the common carotid to the femoral arteries. PA12-induced vasoconstriction displayed a potency gradient, with greatest constriction observed in vessels closest to the heart, with potency reduced and eventually lost further from the heart. PA12-induced vasoactivity was shown to be dependent upon both chymase and ACE1 activity, with ACE1 regulating PA12 activity with greater potency. The intracellular pathways stimulated in response to PA12 were defined using western blotting, with PA12 stimulating phosphorylation of ERK1/2, JNK, p38 and PKCα/β₁₁, but having no influence on PKCδ/θ. Stimulation of these pathways is consistent with the observed PA12-induced vasoconstriction, and also indicates that PA12 activation of AT₁R and the subsequent cytokines, could potentially stimulate hypertrophy, apoptosis, cell growth and differentiation, and inflammation, promoting cadiovascular remodelling and progressing atherosclerosis, hypertension and other vascular diseases if not sufficiently regulated. Taken together, these studies indicate PA12 may have a primary role within the local, tissue-based RAS, providing an alternate substrate to angiotensin I, while ACE1 is the primary regulatory enzyme within the circulation. Our findings also display the chymase-dependent PA12/AT₁R pathway as potential novel targets for pharmacological inhibition of RAS activity to ameliorate hypertension and maladaptive vascular remodelling.
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Bryson, Shona H. "Human anti-(bovine milk fat globule membrane) antibodies : involvement in coronary heart disease." Thesis, University of Bath, 1989. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328539.
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Dean, David C. "Apoptosis in the isolated perfused rat heart, involvement of reperfusion, oxidants and protein synthesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq26315.pdf.
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Knezevic, Tijana. "TRANSLATIONAL APPROACH TO INVESTIGATE INVOLVEMENT OF BAG3 IN PROTEIN QUALITY CONTROL AND HEART FAILURE." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/374885.
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BiologyPh.D.
Heart failure continues to be a global problem, even with all the drugs currently available, leading to a need of new therapeutics to decrease incidence of heart failure. Heart failure is the inability of the heart muscle to pump sufficient blood and oxygen to the rest of the body. One of the causes of heart failure is cardiomyopathy, where cardiac muscle becomes larger and weaker. Genetic mutations in genes encoding sarcomeric, structural and cytoskeletal proteins were found in families that developed cardiomyopathy. Our laboratory has indentified a family with heart failure in whom a novel mutation in the BCL2-associated athanogene 3 (BAG3) has been characterized. Among other cardiomyopathy-causing BAG3 mutations reported in various laboratories. Several BAG3 mutations in humans are known to cause familial dilated cardiomyopathy, myofibrilar myopathy, and giant axonal neuropathy. BAG3 is a stress induced co-chaperone protein that interacts with several heat shock proteins and acts as an important regulator of protein quality control. Expression of BAG3 is high in cardiac, skeletal and smooth muscle. BAG3 is localized at the z-disk of cardiomyocytes and was shown to be essential in keeping a normal assembly of z-disk proteins during mechanical stretch. Interaction of BAG3 with actin capping protein CapZbeta1 prevents degradation of CapZbeta1 via proteasome system and maintains the integrity of the z-disk. BAG3 was shown to promote clearance of misfolded proteins, such as filamin C, via autophagy. Not only that BAG3 is able to promote clearance of dysfunctional filamin C, but it was found to enhance synthesis of the new filamin. BAG3 deficient mice develop fulminant myopathy and cardiomyopathy with disorganization of z-disk and die after one month of age. Not only that BAG3 is involved in myofibrilar stability in the cardiomyocytes and that patients with BAG3 mutations develop cardiomyopathy, but our lab showed that patients with heart failure have decrease levels of BAG3. Since heart failure patients have decreased levels of BAG3, the therapy where BAG3 levels are restored to normal levels may improve heart function. Here, I show that in mouse model of heart failure after MI left ventricle function is restored after administration of AAV9 BAG3. BAG3 overexpression in mouse heart helped the stability of z-disk proteins after mechanical stress and myocardial infarction. Overexpressed BAG3 localizes to z-disk and is also able to increase autophagy in cardiomyocytes and help with clearance of misfolded proteins. Taken together, this study shows that BAG3 is a valid and promising new therapeutic target for heart failure patients. BAG3 overexpression is able to induce autophagy and help the heart cope better with stress. Also, AAV9 vector is robustly expressed in the heart after systemic administration, and is a promising vector for gene delivery in the patient heart.
Temple University--Theses
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Näsström, Lena. "Participation in heart failure home-care : Patients’ and partners’ perspectives." Doctoral thesis, Linköpings universitet, Avdelningen för omvårdnad, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-117095.
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Introduction: Patient participation is important for improving outcomes and respecting selfdetermination and legal aspects in care. Heart failure is a chronic condition that puts high demands on self-care and patient participation. Patients often need advanced care due to deterioration of their heart failure symptoms, and one option is to provide care as home-care. There is limited knowledge of how patients with heart failure and their partners view participation in home-care. Aim: The overall aim of this thesis was to describe different perspectives of participation in structured heart failure home-care among patients with heart failure and their partners. Methods: All patients in this thesis received structured heart failure home-care, according to a model aiming to facilitate care, where safety, participation, and gaining knowledge about the illness and treatment, are in focus. Study I had a prospective pre-post longitudinal design including 100 patients with heart failure receiving home-care. Data was collected by selfadministered questionnaires. Study II had a descriptive design. Nineteen patients receiving home-care were interviewed, and data was analysed using qualitative content analysis. Study III had a descriptive and explorative design. Data was collected by video-recorded observations of 19 home visits and analysed by qualitative content analysis. Study IV had a parallel convergent mixed-method design including 15 partners of patients receiving structured home-care. Data was collected by interviews and self-administered questionnaires. Datasets were first analysed separately and then together. Results: Better self-care behaviour was significantly associated with all measured aspects of participation. Participation by received information increased significantly during the 12-month follow-up (I). Patients’ descriptions of participation included communication between patients and health care professionals, access to care, active involvement in care, a trustful relation with health care professionals, and options for decision-making(II). Observed care encounters revealed that participation was made possible by; (i) interaction, including exchange of care-related information, care-related reasoning, and collaboration, (ii) an enabling approach, including the patient expresses own wishes and shows an active interest, and the nurse is committed and invites to a dialogue (III). Partners scored fairly positive for their participation in care and they performed different levels of caregiving tasks. Descriptions of participation included; adapting to the caring needs and illness trajectory, mastering caregiving demands, interacting with care providers, and gaining knowledge to comprehend the health situation. The mixed-method results showed both convergent results and expanded knowledge (IV). Conclusions: Structured heart failure home-care facilitated participation both for patients and their partners. Patient participation with regard to received information improved significantly after receiving home-care. Aspects of patient participation were consistently associated with better self-care behaviour. Patients’ and partners’ descriptions revealed many aspects of participation, and observed home visits revealed how interaction and an enabling approach underpinned participation.
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Harley, Margaret Pauline. "Touching the heart : an exploration of business involvement with young people in recovery from substance abuse /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19405.pdf.
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Windt, Leon Johannes de. "Ischemia and reperfusion-induced damage of the isolated mouse heart involvement of type IIA secretory phospholipase A2 /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=6892.
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Larsson, Annika. "Medin amyloid - a matter close to the heart : Studies on medin amyloid formation and involvement in aortic pathology." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9275.
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Amyloidoses are a group of protein misfolding diseases characterized by deposits of insoluble fibrillar protein aggregates. Medin amyloid, which is the focus of this thesis, appears in the media of the thoracic aorta in nearly all individuals over 50 years. The fibrils are derived from a 50 amino acid residue fragment of the precursor protein lactadherin. How medin amyloid arises is unknown, but in paper I we demonstrated, with immunohistochemical and in vitro binding experiments, that both lactadherin and medin interact with elastin, implying that the elastic fibre is central in amyloid formation. In paper II, we further showed that the last 18-19 amino acid residues constitute the amyloid-promoting region. In paper III, the consequence of medin deposition was investigated. Aortic specimens from patients with thoracic aorta aneurysm and dissection were examined for medin content. The tissue findings indicated that the two disease groups contained more medin oligomers than normal aortas. Interestingly, recent reports demonstrate that the toxicity of amyloid proteins is attributed to prefibrillar oligomeric aggregates rather than to mature fibrils. In support of this finding, we observed that prefibrillar medin, in contrast to medin fibrils, was toxic in cell culture. Amyloid formation is a nucleation-dependent process. Addition of preformed fibrils to an amyloid protein solution dramatically accelerates fibrillation, a phenomenon called seeding. In paper IV, serum amyloid A-derived (AA) amyloid was found co-localized with medin deposits in the aorta. In vitro, medin fibrils enhanced the formation of AA fibrils, indicative of a seeding mechanism. The data are of great importance as they suggest that one type of amyloid is capable of inducing fibrillation and deposition of another amyloid type. In conclusion, the results of this thesis shed light on how medin is formed, the function of lactadherin and the consequences of medin deposition for aortic pathology.
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Keyser, Rowena J. "Identifying ligands of the C-terminal domain of cardiac expressed connexin 40 and assessing its involvement in cardiac conduction disease." Thesis, Link to online version, 2007. http://hdl.handle.net/10019/651.
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Ng, Dominic Chi Hiung. "Characterizing intracellular signaling mechanisms involved in the progression of cardiac hypertrophy and failure : involvement of JAK/STAT and MAPK pathways." University of Western Australia. Biochemistry and Molecular Biology Discipline Group, 2003. http://theses.library.uwa.edu.au/adt-WU2003.0032.
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[Truncated abstract] The innate ability of the heart to compensate for an increase in workload as a result of disease or injury, through an increase in size and mass is known as cardiac hypertrophy. The hypertrophy of the heart compensates for an increase in workload with an increase in cardiac output. However, excessive hypertrophy can result in cardiac dysfunction and substantially increases the risk of cardiac failure and mortality. The molecular mechanisms that regulate the development of cardiac hypertrophy and cardiac failure are not entirely understood. Traditionally, the G-protein Coupled Receptor (GPCR) and the downstream Mitogen-Activated Protein Kinase (MAPK) family of proteins have been implicated. However, elevated circulating and ventricular levels of several classes of cytokines also suggested that signaling by the downstream effectors of cytokine receptors, such as the Signal Transducers and Activators of Transcription (STATs), may be important. The aim of this thesis was, therefore, to characterize the involvement of MAPK and STAT pathways in regulating cardiac hypertrophy and cardiac failure. A function for MAPK and STAT signaling in regulating cardiac hypertrophy stimulated by the inflammatory cytokine IL-1Β was initially defined in primary cultures of neonatal rat cardiac myocytes. In this study, it was demonstrated that the chemical inhibition of ERK or p38MAPK was sufficient to inhibit IL-1Β-stimulated ANF expression. In contrast, simultaneous inhibition of both ERK and p38MAPK was required to ablate the hypertrophic morphology of cardiac myocytes treated with IL-1Β. These results demonstrated differential signaling from the MAPK isoforms in regulating the gene expression and morphological components of cardiac hypertrophy. In addition, it was revealed that IL-1Β treatment resulted in a delayed response (>60 min) in STAT3α tyrosine phosphorylation, which was subsequently shown to require the initial rapid activation of either ERK or p38MAPK. IL-1Β-stimulated STAT3 phosphorylation was also dependent on the de novo synthesis of secondary signaling molecules. The ablation of the STAT3 tyrosine phosphorylation by the inhibition of ERK or p38MAPK activity, correlated with the attenuation of IL-1Β-stimulated ANF expression, suggesting that signaling through STAT3α may be involved in regulating gene expression associated with IL-1Β cardiac hypertrophy
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Atsalakis, Mihalis. "Prediction of initial involvement of first grade Greek school children in an out-of-school, organized, community physical activity programme : an application of the theory of planned behaviour." Thesis, University of Hull, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262408.
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Foster, Cerrone R., Laura L. Daniel, Christopher R. Daniels, Suman Dalal, Mahipal Singh, and Krishna Singh. "Deficiency of Ataxia Telangiectasia Mutated Kinase Modulates Cardiac Remodeling Following Myocardial Infarction: Involvement in Fibrosis and Apoptosis." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/8570.
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Ataxia telangiectasia mutated kinase (ATM) is a cell cycle checkpoint protein activated in response to DNA damage. We recently reported that ATM plays a protective role in myocardial remodeling following β-adrenergic receptor stimulation. Here we investigated the role of ATM in cardiac remodeling using myocardial infarction (MI) as a model. Methods and Results: Left ventricular (LV) structure, function, apoptosis, fibrosis, and protein levels of apoptosisand fibrosis-related proteins were examined in wild-type (WT) and ATM heterozygous knockout (hKO) mice 7 days post-MI. Infarct sizes were similar in both MI groups. However, infarct thickness was higher in hKO-MI group. Two dimensional M-mode echocardiography revealed decreased percent fractional shortening (%FS) and ejection fraction (EF) in both MI groups when compared to their respective sham groups. However, the decrease in %FS and EF was significantly greater in WT-MI vs hKO-MI. LV end systolic and diastolic diameters were greater in WT-MI vs hKO-MI. Fibrosis, apoptosis, and α-smooth muscle actin staining was significantly higher in hKO-MI vs WT-MI. MMP-2 protein levels and activity were increased to a similar extent in the infarct regions of both groups. MMP-9 protein levels were increased in the non-infarct region of WT-MI vs WT-sham. MMP-9 protein levels and activity were significantly lower in the infarct region of WT vs hKO. TIMP-2 protein levels similarly increased in both MI groups, whereas TIMP-4 protein levels were significantly lower in the infarct region of hKO group. Phosphorylation of p53 protein was higher, while protein levels of manganese superoxide dismutase were significantly lower in the infarct region of hKO vs WT. In vitro, inhibition of ATM using KU-55933 increased oxidative stress and apoptosis in cardiac myocytes.
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Balakrishnan, Meenakshi Puthucode. "Studies on a novel human cardiospecific transcription factor and its involvement in Omi/HtrA2 mediated cell death." Doctoral diss., University of Central Florida, 2010. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4649.
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Omi/HtrA2 is a mitochondrial serine protease that is known to translocate to the cytoplasm upon induction of apoptosis and to activate caspase-dependent and caspase-independent cell death. The molecular mechanism of Omi/HtrA2's function is not clear but involves degradation of specific substrates. These substrates include cytoplasmic, mitochondrial, as well as nuclear proteins. We have pubmedisolated a new Omi/HtrA2 interactor, the THAP5 protein. THAP5 is a fifth member of a large family of transcription factors that are involved in cell proliferation, apoptosis, cell cycle control, chromosome segregation, chromatin modification and transcriptional regulation. THAP5 is an approximately 50kDa nuclear protein, with a restricted pattern of expression. Furthermore, there is no mouse or rat homolog for this protein. THAP5 mRNA is highly expressed in the human heart but some expression is also seen in the brain and skeletal muscle. The normal function of THAP5 in the heart or heart disease is unknown. THAP5 protein level is significantly reduced in the myocardial infarction (MI) area in the heart of patients with coronary artery disease (CAD). This part of the heart sustains most of the cellular damage and apoptosis. Our data clearly show that THAP5 is a specific substrate of the proapoptotic Omi/HtrA2 protease and is cleaved and removed during cell death. The molecular mechanism of THAP5's function is unclear. THAP5 can bind to a specific DNA sequence and repress transcription of a reporter gene. Our work suggests that THAP5 is a tissue specific transcriptional repressor that plays an important role in the normal function of the human heart as well as in the development of heart disease.ID: 029050522; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Thesis (Ph.D.)--University of Central Florida, 2010.; Includes bibliographical references (p. 68-79).
Ph.D.
Doctorate
Burnett School of Biomedical Sciences
Medicine
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Sjöstrand, Håkan. "Erfarenheter från införande av personcentrerad vård på en hjärtavdelning : En studie om effekter och upplevelser av ett förbättringsarbete med syftet att öka patientdelaktighet på hjärtavdelningen vid medicinkliniken i Växjö." Thesis, Hälsohögskolan, Högskolan i Jönköping, The Jönköping Academy for Improvement of Health and Welfare, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:hj:diva-37339.
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Inledning: En nyligen publicerad rapport visar att patientdelaktigheten i Sverige på flera sätt är låg i jämförelse med andra jämförbara länder. Personcentrering är ett förhållningssätt syftande till att öka patientdelaktighet och som i studier visat sig ha positiva hälsoeffekter. Vårdbehovet kan minskas framför allt för patienter med kroniska åkommor såsom hjärtsvikt vilket är den enskilt vanligaste orsaken till inneliggande vård i Sverige. Syfte: Syftet med förbättringsarbetet var att införa ett personcentrerat arbetssätt och därigenom öka patienternas delaktighet på en kardiologisk vårdavdelning. Syftet med studien av förbättringsarbetet var att undersöka personalens upplevelse av detta. Fynden skulle kunna underlätta vidare införande av denna arbetsmetod. Metod: Förbättringsarbetet bedrevs i projektform och genomfördes enligt Nolans förbättringsmodell. Ronden ersattes med ett fördjupat inskrivningssamtal varvid en skriftlig vårdplan upprättades. Patienterna fick skatta upplevd delaktighet i samband med hemgång. Personalens upplevelse studerades med induktiv kvalitativ ansats genom fokusgruppsintervjuer. Resultat: Enligt enkäterna var upplevelsen av delaktighet hög såväl före som efter införandet av personcentrerat arbetssätt, men variationen var stor. Samtliga yrkeskategorier tyckte arbetssättet gav mervärde, både för patienter och personal. Främst betonades ökad patientdelaktighet, bättre förståelse för sammanhanget, ökad teamkänsla och bättre framförhållning. Slutsats: Upplevelsen av införande av personcentrerad vård var allmänt positiv och skiljde sig inte mellan de olika yrkesgrupperna. Personal såg värde av ökad patientdelaktighet, bättre framförhållning samt ökad samstämmighet och samhörighetskänsla med ett personcentrerat arbetssätt.Introduction: A recent published report shows that patient involvement in Sweden is in several ways low compared with other comparable countries. Person-centering is an attitude aimed at increasing patient involvement and which in studies has shown positive health effects. The need for care can be reduced especially for patients with chronic diseases such as heart failure, which is the single most common cause of inpatient care in Sweden. Purpose: The purpose of the improvement work aimed at introducing a person-centered approach and thereby increase the patient's involvement in a cardiac care department. The purpose of the study of the improvement work was to investigate the staff's experience of this. The findings could facilitate further implementation of this method of work. Method: Improvement work was conducted in a project form and implemented according to Nolan's improvement model. The round was replaced with an in-depth enrollment interview, and a written care plan was established. Patients were asked to rate their perceived involvement at time for discharge. The staff's experience was studied with inductive qualitative approach through focus group interviews. Result: According to the surveys, the experience of involvement was high both before and after the introduction of person-centered work methods, but the variation was high. All occupational categories thought the person-centered approach had added value, both for patients and staff. The main emphasis was on increased patient participation, better understanding of the context, increased team spirit and better advancement. Conclusion: The experience of introducing person-centered care was generally positive and did not differ between the different occupational groups. The staff saw value of increased patient involvement, better long term planning and increased coherence and sense of togetherness with a person-centered approach.
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Huber, Adrian Thomas. "Multi-organ non-invasive tissue characterization of fibrosis, adipose tissue, edema and inflammation with magnetic resonance (MR) imaging : applications to myocardium, skeletal muscle and liver interactions Cardiac MR strain: a noninvasive biomarker of fibro-fatty remodeling of the left atrial myocardium Comparison of MR T1 and T2 mapping parameters to characterize myocardial and skeletal muscle involvement in systemic Idiopathic Inflammatory Myopathy (IIM) Non-invasive differentiation of acute viral myocarditis and idiopathic inflammatory myopathy with cardiac involvement using magnetic resonance imaging T1 and T2 mapping CT predicts liver fibrosis: Prospective evaluation of morphology- and attenuationbased quantitative scores in routine portal venous abdominal scans." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS135.
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Cette thèse réalise une preuve de concept pour quantifier la déformation de l’oreillette gauche (OG) en IRM, ainsi que la relaxométrie IRM dans le myocarde, dans les muscles squelettiques et dans le foie. Grâce à l’interaction entre radiologues et ingénieurs, deux logiciels différents ont été développés, appliqués et validés pour l'analyse de la déformation myocardique multi-chambre et pour la cartographie quantitative du T1 multi-organes. La première publication a montré une forte corrélation de la déformation de l’OG, avec le degré de remplacement fibro-graisseux en histologie. Ce biomarqueur d'imagerie fonctionnelle est prometteur, puisque le remodelage structurel du myocarde est un substrat morphologique connu du dysfonctionnement électro-physiologique et de la fibrillation atriale. La deuxième publication a démontré l'influence de la composition et de la vascularisation de différents tissus sur les paramètres cartographiques T1. ΔT1 (prise de contraste musculaire relative) et EHF (prise de contraste musculaire normalisée par la prise de contraste dans le sang) ont été introduits comme alternatives simples au volume extracellulaire (ECV). Dans la troisième publication, les paramètres de relaxométrie appliqués aux muscles squelettiques ont permis une discrimination entre patients avec myocardite aiguë et patients avec des myosites systémiques. La quatrième publication a introduit le T1 du foie pour quantifier l’insuffisance cardiaque chez des patients avec des cardiomyopathies idiopathiques dilatées, montrant de meilleures performances que les paramètres fonctionnels établis tels que les volumes, la fraction d'éjection ou la déformation myocardiqueThis thesis provides a proof of concept for MR atrial strain, as well as MR relaxometry in the myocardium, in skeletal muscles and in the liver. Thanks to a close interaction between radiologist and software engineers, two different softwares were developed, applied and validated: one for multiorgan T1 mapping in the myocardium, skeletal muscle and liver, another one for cardiac four-chamber strain analysis and volumetry. The first publication showed a strong correlation of LA strain with the degree of fibro-fatty replacement in histology. Such functional imaging biomarker in combination with LA volumetry could help to guide clinical decisions, since myocardial structural remodeling is a known morphologic substrate of LA dysfunction, atrial fibrillation and adverse outcome. In the second publication, MR relaxometry parameters applied to the myocardium and skeletal muscles in IIM patients and healthy volunteers were used as a model to demonstrate influences of different tissue composition and vascularization on T1 mapping parameters. ΔT1 and EHF were introduced as simple alternatives to ECV in highly vascularized tissues such as the myocardium. In the third publication, MR relaxometry parameters applied to the skeletal muscls allowed for an accurate discrimination of AVM and IIM with cardiac involvement. However, when applied to the myocardium, parametric mapping did not separate between the two groups. The fourth publication introduced native T1 of the liver an easily accessible and accurate non-invasive imaging associate of congestive HF in IDCM patients with better performance than established functional parameters such as LV volumes, ejection fraction or strain
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Panjwani, Naveed Nooruddin. "The involvement of heat shock proteins in MHC class II antigen processing and presentation." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391439.
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Dufresne, Philippe. "Involvement of poly (A)-binding and heat shock 70 kDa proteins in «Turnip mosaic virus» infection." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21945.
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Viruses are obligate intracellular parasites. Most possess small genomes with a limited coding capacity, which means that they rely on host factors for the completion of their life cycle. The recruitment of cellular proteins is essential as in their absence viruses cannot replicate effectively. Tandem affinity purification was used in Arabidopsis thaliana to identify host interactors of Turnip mosaic virus (TuMV) RNA-dependent RNA polymerase (RdRp). The heat shock cognate 70-3 (Hsc70-3) and poly(A)-binding (PABP) proteins were recovered and shown to interact with the RdRp in vitro. As previously shown for PABP, Hsc70 was redistributed to nuclear and membranous fractions from infected plants and both RdRp interactors were co-immunoprecipitated from a membrane-enriched extract using RdRp specific antibodies. Fluorescently-tagged RdRp and Hsc70-3 localized to cytoplasm and nucleus when expressed alone or in combination in Nicotiana benthamiana. However, when co-expressed with TuMV membrane binding protein 6K-VPg-Pro, they were redistributed to large perinuclear vesicles where replication takes place. Thus, Hsc70-3 and PABP2 are potentially integral components of the replicase complex and could have important roles to play in potyviral RdRp functions. To further characterize the role of PABP in potyvirus infection single and double gene knockouts were isolated and characterized for all high expressing class II PABP genes in Arabidopsis thaliana: PAB2, PAB4 and PAB8, all of which were found to be viable and fertile. Whereas single knockout plants, for the most part, demonstrate a normal phenotype, pab2 pab4 and pab2 pab8 double mutants had important debilitations in regard to the growth and development of both vegetative and reproductive organs. Experiments with these PABP deficient plants indicate that partial PABP depletion in A. thaliana, although not sufficient to confer complete resistance, can impede replicative cycle of TuMV in the cell. TuMV replication in theLes virus sont des parasites intracellulaires stricts. La plupart possèdent de petits génomes ayant une capacité d'encodage limitée et dépendent conséquemment des facteurs de l'hôte pour compléter leur cycle d'infection. Le recrutement de ces protéines est essentiel à leur réplication. Nous avons utilisé une stratégie de purification en tandem dans Arabidopsis thaliana dans le but d'identifier les protéines de l'hôte interagissant avec la polymérase virale à ARN (RdRp) du virus de la mosaïque du navet (TuMV). Les protéines Hsc70-3 et PABP ont été purifiées et leur interaction avec la RdRp confirmée in vitro. Tel que rapporté pour la PABP, la Hsc70 s'est retrouvée redistribuée aux fractions nucléaires et membranaires dans des plants infectés. De plus, nous avons été en mesure de co-immunoprécipiter ces deux protéines dans un extrait membranaire avec un anticorps anti-RdRp. Lorsqu'exprimées seules ou ensemble dans Nicotiana benthamiana, la RdRp et la Hsc70-3 localisèrent au cytoplasme et au noyau. Par contre, lorsque co-exprimées avec le polypeptide 6K-VPg-Pro du TuMV, elles se trouvèrent redistribuées à l'intérieur d'une vésicule périnucléaire là où le virus se réplique. Hsc70-3 et PABP2 sont donc potentiellement des protéines faisant partie du complexe de réplication et ont probablement un rôle important à jouer dans les fonctions de la RdRp. Afin de déterminer le rôle de la PABP dans le cycle de réplication des potyvirus, nous avons généré des mutants d'A. thaliana knockout simple ou double pour tous les gènes de PABP de la classe II; PAB2, PAB4 et PAB8. Alors que les mutants simples présentent un phénotype normal, les mutants double pab2 pab4 et pab2 pab8 ont des déficiences de croissance et de développement. Les expériences menées avec ces plants indiquent qu'une déplétion partielle des niveaux de PABP, quoique étant insuffisante pour mener à un phénotype de résistance complet, inhibe le cycle
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Honzawa, Yusuke. "Involvement of interleukin-17A-induced expression of heat shock protein 47 in intestinal fibrosis in Crohn's disease." Kyoto University, 2014. http://hdl.handle.net/2433/189671.
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Alford, Kate Alexandra. "Investigation by RNA interference of the involvement of heat shock protein 27 and HuR in inflammatory gene expression." Thesis, Imperial College London, 2006. http://hdl.handle.net/10044/1/11277.
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Reynolds, Rema Ella. "Holla if you hear me giving voice to those we have missed : a qualitative examination of black middle class parents' involvement and engagement activities and relationships in public secondary schools /." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1835603611&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Mogaji, Emmanuel. "Emotional appeals in UK banks' print advertisement." Thesis, University of Bedfordshire, 2016. http://hdl.handle.net/10547/622103.
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The unprecedented turbulence and uncertainty experienced in global economic and financial markets because of the 'credit crunch' has had a damaging impact on consumer confidence. Trust and credibility have been eroded as many customers feel let down by the banks suggesting the need for banks to rebuild constructive dialogue and long-term, meaningful relationships with their customers again. Though financial service, in this case, is considered a utilitarian service, based on the fact that money is needed to support people‘s daily activities, the present state of financial service has suggested the need for banks to appeal to consumers‘ emotions with the aim of improving their reputation. Also, the competition within the industry also could suggest the need to adopt an emotionally appealing advertisement strategy as emotions are known to play an influential role in building robust brand preference. This study builds on the communication theory, meaning transfer theory and consumer involvement theory, to understand the messages the banks are sending out and to elicit consumers‘ emotional reaction. One thousand, two hundred and seventy-four UK bank advertisements in nine national newspapers were content-analysed to identify the emotional appeals presented by the banks. The perception of these appeals and their associated meanings were sought through semi-structured interviews with 33 participants in London and Luton. The results of the analysis indicated that UK Banks are utilising emotional appeal in their advertisements to reach out to the consumers to convince them to upgrade their account, to open an additional account or switch their account. The most predominantly used appeals were relief and relaxation followed by excitement and happiness or satisfaction with the bank, and finally, security and adventure. However, variations were found in different financial products that employed emotional appeals. It was found that high-involvement products such as mortgages and loans used fewer emotional appeals. Both bank groups - high street banks, including the big four (Barclays, HSBC, Lloyds and RBS) and non-high street banks, such as the new entrants, supermarket brands, and online banks were using emotional appeals. However, it is acknowledged that the communication strategies between these banks could be different as the non-high street banks are more likely to repeat and publish the same messages across many newspapers, instead of publishing different emotionally appealing advertisements. Though consumers acknowledged these emotional appeals in the advertisements, they were more concerned about their relationship with the banks as they don‘t rely on advertisements to make a financial decision. Rather, recommendations from families, friends and associates and also branch location are more important when deciding on which bank to choose. The lack of congruency between financial services and emotional appeals in advertisements is also observed as customers are more likely to be persuaded by rational appeals however this study has not completely ruled out emotional appeals in bank advertisements as the use of both types of appeals is recommended. The study provides important theoretical and managerial contributions to understanding how the consumers understand meaning-embedded advertisements produced by the banks. Managers will be able to consider the implications of advertisements in enhancing their brand equity and building relationships with customers in anticipation that, by word of the mouth and established relationship, their bank‘s reputation will be enhanced. Limitations of the study and opportunities for future research are identified.
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C, Bruni. "To develop a definition and validated expert recommendations to diagnose primary heart involvement in systemic sclerosis - preliminary pathway to a T2T approach." Doctoral thesis, 2022. http://hdl.handle.net/2158/1264311.
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Systemic sclerosis related primary heart involvement (SSc-pHI) is a leading cause of morbidity and mortality during the disease course. Despite the availability of Expert opinion papers on its detection and evaluation, there is heterogeneity regarding its definition, as well as granularity of data regarding the use of diagnostic tests for its evaluation in SSc. The aim of our study was to create a data- and consensus-driven definition of SSc-pHI and start its valiidation process. Consequently, we aimed at creating a consensus guidance to support clinicians in the screening, diagnosis and monitoring of SSc-pHI. Finally we applied the Consensus guidance retrospectively in a real-life cohort of SSc patients.
Two different systematic literature reviews (SLRs) were carried on, the first aimed at identifying the different features of the possible manifestations of SSc-pHI, the second at gathering information on the diagnostic tests and related parameters used for the evaluation of cardiac involvement. The data derived from the two SLRs were used in Expert meetings, including specialists from the rheumatology, immunology, cardiology, pathology fields, as well as a patient research partner. The first meeting lead to the creation of a definition of SSc-pHI, which was partially validated for faesibility, criterion validity and reliability. The subsequent five meetings lead to the creation of a consensus guidance, composed of overarching principles and guidance statements, covering both the screening, diagnosis and monitoring assessments of SSc-pHI. In addition, SSc-specific echocardiography and cardiac magnetic resonance protocols were proposed, both for clinical core assessments and for optional/research agenda evaluations. The real-life retrospective evaluation of the Consensus guidance showed the added value of identifying at risk SSc-patients and regularly applying screening/diagnostic core evaluations, supporting their role in the detection of SSc-related cardiac events and complications. Future steps will include the prospective application of the consensus statements and the proposed ecocardiography/cardiac magnetic resonance protocol, leading the basis for a standardized detection of SSc-pHI and future testing of medications for its prevention and treatment.
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Pinho, Marta Andreia de Ribeiro. "Myocardial effect of Intermedin in hypertrophic heart: mechanisms and involvement of endothelial dysfunction." Master's thesis, 2014. https://repositorio-aberto.up.pt/handle/10216/70940.
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Rodrigues, Patrícia Fernandes Dias de Madureira. "Role of cardiac imaging in the evaluation of diseases with unclear heart involvement." Doctoral thesis, 2020. https://hdl.handle.net/10216/130307.
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Rodrigues, Patrícia Fernandes Dias de Madureira. "Role of cardiac imaging in the evaluation of diseases with unclear heart involvement." Tese, 2020. https://hdl.handle.net/10216/130307.
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Pinho, Marta Andreia de Ribeiro. "Myocardial effect of Intermedin in hypertrophic heart: mechanisms and involvement of endothelial dysfunction." Dissertação, 2014. https://repositorio-aberto.up.pt/handle/10216/70940.
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Prosser, H. C. G. "Involvement of novel cardiac peptides in healthy and ischemic hearts : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Biology at the University of Canterbury /." 2009. http://hdl.handle.net/10092/2731.
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Lin, Yi-Ching, and 林宜靚. "Work with Your Heart - Exploring the Relationships Among Job Autonomy, Psychological Capital, Perceived Supervisor Support and Job Involvement." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/mc7ekk.
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碩士國立臺北大學
企業管理學系
104
This study explored the relationships among an individual’s job autonomy, psychological capital (PsyCap), perceived supervisor support, and job involvement. First, we examined the relationship between job autonomy and job involvement, the relationship between job autonomy and PsyCap, and the relationship between PsyCap and job involvement. Second, we investigated if PsyCap has a mediating effect on the relationship between job autonomy and job involvement. Last, we tested whether perceived supervisor support has a moderating effect on the relationship between job autonomy and job involvement. Our study used convenience sampling and snowball sampling to collect Taiwan’s general workers; in addition, most of our data were in north of Taiwan, and some of them were in other area of Taiwan. We distributed 318 paper-based questionnaires in four months and received 234 valid copies; hence, the valid returned rate was 73.58%. After using hierarchical regression to analyze the data, the results showed that job autonomy had a positive effect on job involvement, job autonomy had a positive effect on PsyCap, and PsyCap had a positive effect on job involvement. For testing the mediating and moderating effect, the result explained that PsyCap fully mediated the relationship between job autonomy and job involvement; perceived supervisor support positively moderated the relationship between job autonomy and job involvement. From the result, we could understand that PsyCap has a powerful effect on an individual’s job involvement. In addition, perceived supervisor support would enhance the positive relationship between job autonomy and job involvement. At the end, our study provided discussion, theoretical implications, management implications, limitations, and recommendations for future study and management.
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Yeh, Han-Pin, and 葉漢斌. "Reward of service heart: Moderation of social support, emotional intelligence, and job involvement on consequences of emotional labor." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/39836117432742322524.
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碩士國立屏東科技大學
企業管理系所
95
Service often is performed by service action blueprint, service providers are like actors and the service process is like a show. In such a “show” performance, service providers' emotion is an important key to interact with customers. Previous studies focus merely on the impact of service provider’s own psychological state and behaviors. There has been limited research on service providers' personal characteristics and work attitude's effects on emotional state and customer's behaviors. Therefore the purpose of this study is to examine moderate effect on service provider’s emotion intelligence, job involvement, and social support in emotion labor and emotion exhaust, service orient organization citizen behavior, and customer behavior intention. The sample is drawn from front-line service providers in Kaohsiung and Pingtung area. To avoid common method variance (CMV), paired survey was commenced. The questionnaire was distributed to the service providers and three to five of their own customers. In total 1323 valid samples were collected. Key research findings are: (1) Emotion labor positively affects emotion exhaust, service orient organization citizen behavior, and customer behavior intention. (2) Emotion intelligence positively moderating the effect between emotion labor and emotion exhaust. (3) Job involvement positively moderating the effect between emotion labor and service orient organization citizen behavior, and customer behavior intention. (4) Different service objects ("people" or "things" as main objects) show significant difference on the moderation effect. Based on the research findings, managerial and research implication are discussed.
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Wolter, Jessica Ilona [Verfasser]. "Pharmacological preconditioning of the rat heart by Xenon and Isoflurane : involvement of PKCe, p38 MAPK and Hsp 27 / vorgelegt von Jessica Ilona Wolter." 2006. http://d-nb.info/983357714/34.
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Hammad, Maha. "CHARACTERIZATION OF THE ANGIOTENSIN TYPE 1 RECEPTOR AND THE BETA2 ADRENERGIC RECEPTOR PROPERTIES: THE INVOLVEMENT OF ARRESTIN2, RAB1 AND SOME MOLECULAR CHAPERONES IN THE ASSEMBLY AND TRAFFICKING OF GPCRS." 2010. http://hdl.handle.net/10222/13068.
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Current drugs used to treat Congestive Heart Failure target the renin-angiotensin and adrenergic systems. Studies showed increased mortality rates in patients treated with a combination of these medications. Angiotensin-AT1 and ?2-Adrenergic receptors were shown to form receptor heteromers. Blockade of one receptor in the complex can affect the signal transmitted by the other; suggesting that ligand-based therapy is not as selective as we might think. Modulating receptor trafficking after synthesis might prove to be a valid therapeutic strategy. Unfortunately, little is known about receptor assembly and transport from Endoplasmic Reticulum to Plasma Membrane. The objectives of this study are to identify the proteins that participate in the assembly of AT1R-?2AR heteromer and the regulators of the anterograde trafficking of G-Protein Coupled Receptors. This thesis introduces the role of important targets in those poorly understood processes. The identification of such targets could lead to developing better drugs with fewer adverse effects.
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Ker, Walsh Jean. "Do you hear what I hear? Reception in Australian political discourse and effects on engagement with democracy." Thesis, 2016. https://vuir.vu.edu.au/31035/.
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This thesis in political communication details a qualitative investigation into how citizens receive and make sense of political discourse in a twenty-first century democracy. Recognising criticism of the national discourse as ‘dumbed down’, it explores with a cohort of Australian citizens what meaning they receive from contemporary discourse and how it affects their engagement with democracy. The project employs an innovative method of recruiting participants at a polling booth in Australia’s most typical suburb, followed a month later by same day data collection from three wide-scope groups in facilitated discussion. Analysis of the data finds citizens diagnose the discourse as negative and of poor quality, for which they first blame the media. There is an expressed fear that the shallowness of discourse is dumbing them down. In contradiction to their expectations of democratic citizenship, they are powerless to make themselves heard within a discourse which neither recognises nor respects them. They find the discourse alienating, although overwhelming support for compulsory voting militates against democratic dis-engagement. Digital age communications are used to support unstructured democratic engagement and circumvent the banality of local political discourse.