Bakgrund: Hjärtinfarkt är den vanligaste dödsorsaken i Sverige och orsakas oftast av en blodpropp som bildas från en plackruptur i något av hjärtats kranskärl. Risken att drabbas av en hjärtinfarkt ökar med åldern, även faktorer som diabetes, ärftliga anlag, stress, rökning, högt blodtryck och övervikt är riskfaktorer för att drabbas av sjukdomen. Män drabbas oftare av sjukdomen än kvinnor och kvinnors symptom vid insjuknandet kan ibland vara diffusa och det kan vara svårt ställa en diagnos. För att sjuksköterskan skall kunna tillgodose grundläggande behov hos personer med hjärtsjukdom så krävs god kompetens. Målet är att främja hälsa och välbefinnande hos patienten samt att förebygga ohälsa och lindra lidande.       Syfte: Syftet med litteraturstudien var att beskriva kvinnors erfarenheter av vardagen efter en hjärtinfarkt. Vidare var syftet att beskriva de inkluderade artiklarnas datainsamlingsmetod.  Metod: En deskriptiv litteraturstudie bestående av tio vetenskapliga artiklar. Huvudresultat: Resultatet speglar hur kvinnorna på ett fysiskt och känslomässigt sätt påverkas efter insjuknandet. Rädslan som finns hos dem att de skall drabbas av en ny hjärtinfarkt samt behovet av att utföra livsstilsförändringar. Betydelsen av stöd och hjälp från närstående samt hur arbetet påverkas efter insjuknandet. Vikten av beröring och intima relationer och dess betydande del i återhämtningen för kvinnorna.  Slutsats: Efter genomgången hjärtinfarkt har närstående en viktig betydande roll för återhämtningsprocessen. För att bibehålla en god egenvård är det viktigt att kvinnorna får hjälp från kompetent sjukvårdspersonal. Som sjuksköterska är det viktigt att besitta kunskap kring kvinnornas erfarenheter samt om sjukdomen / Background: Myocardial infarction is the most common cause of death in Sweden and is usually caused by a blood clot that formed from a plaque rupture in one of the coronary arteries. The risk of suffering a heart attack increases with age, but also factors such as diabetes, hereditary predisposition, stress, smoking, high blood pressure and obesity are risk factors for developing the disease. Men are affected more often by heart diseases than women, and women's symptoms at onset can sometimes be diffuse to make a diagnosis. The nurse need to be able to meet the basic needs of people with heart disease that requires good skills. The goal is to promote health and well-being of the patient and to prevent illness and relieve suffering. Aim: The aim of this study was to describe how women experiences the everyday life after a heart attack. Furthermore, the aim was to describe the articles included data collection method. Method: A descriptive literature of ten scientific articles. Main Results: The results reflect how the women on a physical and emotional way are affected by the myocardial infarction. They feel a fear that they will suffer a heart attack again and they need to do some lifestyle changes. The support and help from the family, is important for them such as touch and intimate relationships and its significant part in the recovery of women. Conclusion: After myocardial infarction have been related to a major significant role in the recovery process. To maintain a good self-care, it is important that women receive help from skilled health professionals. As a nurse, it is important to have knowledge about women's experiences and about the disease

<p>Radiation therapy can cause acute toxicity and long-term side effects in normal tissues. Because part of the acute toxicity of radiation is due to p53-mediated apoptosis, blocking p53 during irradiation can protect some normal tissues from acute radiation injury and might improve the therapeutic ratio of radiation therapy. However, the mechanisms by which p53 regulates late effects of radiation are not well understood. Here, I utilized genetically engineered mouse models to dissect the role of p53 in regulating two of the most clinically significant late effects of radiation: radiation-induced carcinogenesis and radiation-induced myocardial injury. </p><p> It has been well characterized that mice with one allele of p53 permanently deleted are sensitized to radiation-induced cancer. Therefore, temporary inhibition of blocking p53 during irradiation could promote malignant transformation. Experiments with mice lacking functional p53 in which p53 protein can be temporarily restored during total-body irradiation (TBI) suggest that the radiation-induced p53 response does not contribute to p53-mediated tumor suppression. Here, I performed reciprocal experiments and temporarily turned p53 off during TBI using transgenic mice with reversible RNA interference against p53. I found that temporary knockdown of p53 during TBI not only ameliorated acute hematopoietic toxicity, but in both Kras wild-type and tumor-prone KrasLA1 mice also prevented lymphoma development. Mechanistic studies show that p53 knockdown during TBI improves survival of hematopoietic stem and progenitor cells (HSPCs), which maintains HSPC quiescence and prevents accelerated repopulation of surviving cells. Moreover, using an in vivo competition assay I found that temporary knockdown of p53 during TBI maintains the fitness of p53 wild-type HSPCs to prevent the expansion of irradiated mutant cells. Taken together, our data demonstrate that p53 functions during TBI to promote lymphoma formation by facilitating the expansion of irradiated HSPCs with adaptive mutations. </p><p> p53 functions in the heart to promote myocardial injury after multiple types of stress, including ischemic injury, pressure overload and doxorubicin-induced oxidative stress. However, how p53 regulates radiation-induced myocardial injury, which develops after radiation therapy, is not well understood. Here, I utilized the Cre-loxP system to demonstrate that p53 functions in endothelial cells to protect mice from myocardial injury after a single dose of 12 Gy or 10 daily fractions of 3 Gy whole-heart irradiation (WHI). Mice in which both alleles of p53 are deleted in endothelial cells succumbed to heart failure after WHI due to myocardial necrosis, systolic dysfunction and cardiac hypertrophy. Moreover, the onset of cardiac dysfunction was preceded by alterations in myocardial vascular permeability and density. Mechanistic studies using primary cardiac endothelial cells (CECs) irradiated in vitro indicate that p53 signals to cause a mitotic arrest and protects CECs against radiation-induced mitotic catastrophe. Furthermore, mice lacking the cyclin-dependent kinase inhibitor p21, which is a transcriptional target of p53, are also sensitized to myocardial injury after 12 Gy WHI. Together, our results demonstrate that the p53/p21 axis functions to prevent radiation-induced myocardial injury in mice. Our findings raise the possibility that when combining radiation therapy with inhibitors of p53 or other components of the DNA damage response that regulate mitotic arrest, patients may experience increased radiation-related heart disease. </p><p> Taken together, our results demonstrate crucial but distinct roles of p53 in regulating late effects of radiation: p53-mediated apoptosis promotes radiation-induced lymphomagenesis, but p53-mediated cell cycle arrest prevents radiation-induced myocardial injury. These findings indicate that p53 may generally play a protective role from radiation, particularly at high doses, in cells where p53 activation is uncoupled from the induction of the intrinsic pathway of apoptosis. Therefore, selectively inhibiting p53-mediated apoptosis may be a promising approach to ameliorate acute radiation toxicity without exacerbating late effects of radiation.</p> / Dissertation

Coronary artery bypass graft (CABG) surgery is a common treatment for patients with coronary artery disease. A potential complication of CABG is myocardial ischemia or infarction. In this thesis, a method - based on laser Doppler flowmetry (LDF) - for detection of intra- and postoperative ischemia by myocardial perfusion monitoring is evaluated. LDF is sensitive to motion artifacts. In previous studies, a method for reduction of motion artifacts when measuring on the beating heart has been developed. By using the ECG as a reference, the perfusion signal is measured in intervals during the cardiac cycle where the cardiac motion is at a minimum, thus minimizing the artifacts in the perfusion signal. The aim of this thesis was to investigate the possibilities to use the ECG-triggered laser Doppler system for continuous monitoring of myocardial perfusion in humans during and after CABG surgery. Two studies were performed. In the first study, changes in myocardial perfusion during CABG surgery were investigated (n = 13), while the second study focused on postoperative measurements (n = 13). In addition, an ECG-triggering method was implemented and evaluated. It was found that the large variations in myocardial perfusion during CABG surgery could be monitored with the ECG-triggered laser Doppler system. Furthermore, a perfusion signal of good quality could be registered postoperatively from the closed chest in ten out of thirteen patients. In eight out of ten patients, a proper signal was obtained also the following morning, i.e., about 20 hours after probe insertion. The results show that respiration and blood pressure can have an influence on the perfusion signal. In conclusion, the results indicate that the method is able to detect fluctuations in myocardial perfusion under favourable circumstances. However, high heart rate, abnormal cardiac motion, improper probe attachment and limitations in the ECG-triggering method may result in variations in the perfusion signal that are not related to tissue perfusion. / Varje år utförs omkring 4500 kranskärlsoperationer i Sverige. En allvarlig komplikation som kan uppstå efter operationen är otillräcklig blodförsörjning till hjärtmuskeln. Den här licentiatavhandlingen handlar om utveckling och utvärdering av en metod, baserad på laserdopplerteknik, för att kunna upptäcka nedsatt blodperfusion i hjärtmuskeln på ett tidigt stadium. Laserdopplertekniken är känslig för rörelsestörningar. I tidigare studier har en metod för reducering av rörelsestörningar vid mätning på slående hjärta tagits fram. Med EKG:t som referens mäts blodperfusionen i de faser under hjärtcykeln då hjärtats rörelse är som minst, vilket minskar bidraget av rörelsestörningar i blodperfusionssignalen. I den här avhandlingen undersöks om metoden kan användas för kontinuerlig övervakning av hjärtmuskelns blodperfusion på patienter under och efter hjärtoperationer. Två studier har genomförts: en där hjärtmuskelns perfusion mättes i olika faser under kranskärlsoperationer och en där mätproben lades in i hjärtmuskeln under operationen och mätningar gjordes under det första dygnet efter operationen. Det visade sig vara möjligt att följa förändringar i hjärtmuskelns blodperfusion under operation. Det var även möjligt att registrera en perfusionssignal av god kvalitet efter operationen då bröstkorgen var stängd. Hos åtta av tio patienter erhölls en bra signal även morgonen efter operationen, dvs. ca 20 timmar efter att proben lades in. Resultaten visar också att andning och blodtryck kan ha en påverkan på blodperfusionssignalen. Slutsatsen av arbetet är att det går att se variationer i hjärtmuskelns blodperfusion med EKG-triggad laserdoppler under vissa förutsättningar. Signalen är dock i många fall svårtolkad på grund av att t ex hög hjärtfrekvens, onormal hjärtväggsrörelse eller ändrad probposition sannolikt kan ge variationer i perfusionssignalen som inte är relaterade till blodflödesförändringar. / Report code: LIU-TEK-LIC-2007:35.

Bakgrund: I Sverige är den vanligaste dödsorsaken kranskärlssjukdom, vilket kan innebära hjärtinfarkt. Riskfaktorer för hjärtinfarkt är låg fysisk aktivitet, höga blodfetter, rökning, låg inkomst och låg utbildning. En hjärtinfarkt uppstår vanligtvis på grund av att ett åderförfettningsplack har brustit och bildat en blodpropp.  Syfte: Syftet med denna litteraturstudie är att undersöka kvinnor och mäns erfarenheter efter en hjärtinfarkt. Metod: Nio kvalitativa vetenskapliga studier analyserades enligt Fribergs modell för litteraturöversikt. Resultat: Resultatet sammanställdes i de tre kategorierna Begränsningar i vardagen, Stöd respektive brist på stöd från omgivningen, Förändrad syn på livet.  Konklusion: De personer som drabbats av en hjärtinfarkt lider ofta av hälsoproblem som fatigue i efterförloppet. Livsstilsförändringar kan vara svåra att genomföra och framförallt att bibehålla. Hälso- och sjukvårdspersonal bör vara väl insatta i vad livet efter en hjärtinfarkt innebär och ge gott stöd till de som drabbats. Livsstilsförändringar bör genomföras några få i taget istället för alla på samma gång för att det ska bli hållbart på lång sikt. / Background: The most common cause of death in Sweden is coronary heart disease, which can imply myocardial infarction. Risk factors for myocardial infarction are low physical activity, high blood lipids, smoking, low income and poor levels of education. A myocardial infarction occurs when a fatty, calcified plaque has ruptured and formed a trombosis. Aim: The aim of this literature study is to examine women and men’s experiences after a myocardial infarction. Method: Nine qualitative scientific studies were analyzed according to Friberg’s model for literature review. Results: The results were complied into three categories named Restrictions in daily life, Support or lack of support from the community, Altered life vision. Conclusion: The people who have suffered a myocardial infarction often sustain health problems such as fatigue in the aftermath. Lifestyle changes may be difficult to adopt and above all to maintain. Healthcare professionals should be well informed of what life after a myocardial infarction can implicate and give good support to those affected. Lifestyle changes should be carried out a few at a time rather than all at once to make them sustainable in the long term.

Thesis (MScMedSc)--Stellenbosch University, 2012. / ENGLISH ABSTRACT: Introduction: The worldwide escalation in the incidence of obesity and its strong association with insulin resistance, type 2 diabetes and the cardiovascular complications that accompany these disease states have elicited interest in the underlying mechanisms of these pathologies. Preliminary data generated in our laboratory showed that obesity is associated with abnormalities in the insulin signalling pathway. Specifically, we found a down-regulation of protein kinase B (PKB/Akt), which is known to mediate the metabolic effects of insulin. One of the downstream targets of PKB/Akt is glycogen synthase kinase-3 (GSK-3), which is inhibited by this phosphorylation. Detrimental effects of unopposed activity of GSK-3 have recently been described. This may play a pivotal role in some of the adverse consequences of insulin resistance in the heart. Hypothesis: Chronic inhibition of GSK-3 will induce myocardial hypertrophy or exacerbate the development of existing hypertrophy in a pre-diabetic model of diet induced obesity and insulin resistance. Objectives: (1) Assess the extent of the development of myocardial hypertrophy in a rat model of diet induced obesity (DIO) and insulin resistance. (2) Assess the effect of inhibition of GSK-3 protein on the development of myocardial hypertrophy. Methods: Two groups of age-matched male Wistar rats were used. Control animals received standard rat chow, while obese animals received a high caloric diet for 20 weeks. After 12 weeks, half of the animals in both groups received GSK-3 inhibitor treatment (CHIR118637, 30mg/kg/day, Novartis). At the end of 20 weeks, three series of experiments were conducted. (i) The animals were subjected to echocardiography to determine in vivo myocardial function, and biometric, metabolic and biochemical parameters were evaluated. (ii) The ability of the cardiomyocytes to accumulate deoxy-glucose after stimulation with insulin was determined, and (iii) the localization of key proteins was monitored using fluorescence microscopy and cell size was determined using light microscopy and flow activated cell sorter analysis. Results and discussion: The high caloric diet increased body weight (p<0.005) and intraperitoneal fat mass (p<0.01) when compared to controls. Complications associated with obesity, such as impaired glucose tolerance (p<0.05), hyperinsulinemia (p<0.0005) and an increased HOMA-IR index (p<0.01) were observed. Additionally, cardiomyocytes from the DIO animals had a significantly impaired response to insulin, specifically when 10nM (p<0.05) and 100nM (p<0.05) of insulin were used as stimulus. We also found a dysregulation in PKB/Akt, indicated by a down-regulation of phosphorylated PKB/Akt (p<0.01). The diet promoted the development of myocardial hypertrophy, since the ventricular weight (p<0.05) and ventricular weight to tibia length ratio were increased (p<0.01). Echocardiography experiments showed an increase in end diastolic diameter in the DIO animals (p<0.05). Additionally, there was an increase in the cardiomyocyte cell width in the DIO rats (p<0.0001) and a tendency for peri-nuclear localization of NFATc3. GSK-3 inhibition promoted the development of insulin resistance in control animals, as indicated by an increase in the body weight (p<0.05), serum insulin levels (p<0.01) and HOMA-IR index (p<0.01). In the DIO animals, the GSK-3 inhibitor treatment improved insulin resistance, as a decrease in serum insulin concentration (p<0.05) was observed. The cardiomyocytes from the treated DIO animals also showed an increase in glucose uptake (p<0.05) when stimulated with 100nM of insulin. The GSK-3 inhibitor promoted the development of myocardial hypertrophy in the control animals, indicated by an increase in ventricular weight (p<0.05) and cardiomyocyte cell width (p<0.0001), but did not exacerbate hypertrophy in the DIO animals. Conclusion: Both the high caloric diet and the GSK-3 inhibitor promoted the development of insulin resistance and myocardial hypertrophy in the rats. In the DIO animals the GSK-3 inhibitor treatment ameliorated insulin resistance and did not promote the further development of myocardial hypertrophy. / AFRIKAANSE OPSOMMING: Inleiding: Die huidige styging in vetsugtigheid en die sterk assosiasie daarvan met insulien weerstandigheid, tipe 2 diabetes en kardiovaskulêre komplikasies soos hipertrofie, het ‘n belangstelling in die onderliggende meganismes van hierdie siektetoestande ontlok. Voorlopige data uit ons laboratorium het getoon dat vetsug geassosieerd is met abnormaliteite in die insulien seintransduksie-pad soos byvoorbeeld ‘n afregulering van miokardiale proteïen kinase B (PKB/Akt), wat bekend is om die metaboliese effekte van insulien te medieer. Een van die proteïene wat deur PKB/Akt gefosforileer en daardeur geïnhibeer word, is glikogeen sintase kinase-3 (GSK-3). Negatiewe effekte van onge-opponeerde aktiwiteit van GSK-3 is beskryf en dit mag ‘n sleutelrol speel in sommige van die nadelige gevolge van insulien weerstandigheid in die hart. Hipotese: Chroniese onderdrukking van GSK-3 sal miokardiale hipertrofie ontlok of die bestaande hipertrofie in ‘n pre-diabetiese model van dieet-geïnduseerde vetsug en insulien weerstandigheid vererger. Doelstellings: (1) Om die omvang van die ontwikkeling van miokardiale hipertrofie in ‘n rotmodel van dieet-geïnduseerde vetsug te ondersoek en (2) om die effek van inhibisie van GSK-3 op die ontwikkeling van hipertrofie te ondersoek. Metodes: Ouderdomsgepaarde manlike Wistarrotte is in hierdie studie gebruik. Die diere is vir ‘n periode van 20 weke aan verskillende diëte onderwerp, naamlik standaard kommersiële rotkos vir die kontrole diere en ‘n hoë kalorie dieet vir die eksperimenteel vet diere (DIO). Helfte van elke groep diere is vir 8 weke met ‘n GSK-3 inhibitor behandel (CHIR118637, 30mg/kg/day, Novartis). Na die 20 weke is 3 eksperimentele reekse uitgevoer: (i) Die diere is eggokardiografies ondersoek om in vivo miokardiale funksie te bepaal en biometriese, metaboliese en biochemiese parameters is evalueer. (ii) Die vermoë van kardiomiosiete om de-oksiglukose na insulien stimulasie te akkumuleer, is bepaal, en (iii) die lokalisering van sleutelproteïene is met behulp van fluoressensie mikroskopie en die selgrootte met behulp van ligmikroskopie bepaal. Resultate en bespreking: Die hoë kalorie dieet het gepaard gegaan met ‘n beduidende toename in liggaamsgewig (p<0.005) en intraperitoneale vetmassa (p<0.01) in vergelyking met diere op die kontrole dieet. Newe-effekte geassosieerd met vetsug nl. onderdrukte glucose toleransie (p<0.05), hiperinsulinemie (p<0.0005) en ‘n verhoogde HOMA-IR index (p<0.01) is ook waargeneem. Daar was ook ‘n beduidend ingekorte respons van glukose opname deur kardiomiosiete van die vet diere na stimulasie met 10nM (p<0.05) en 100nM (p<0.05) insulien. Disregulering van PKB/Akt is gevind in die vorm van ‘n afregulering van die fosforilering van die proteïen (p<0.01). Die dieet het ook gelei tot die ontwikkeling van miokardiale hipertrofie aangesien die ventrikulêre gewig (p<0.05) asook die verhouding van die ventrikulêre gewig teenoor tibia lengte beduidend toegeneem het (p<0.01). Eggokardiografie het ‘n toename in ventrikulêre end-diastoliese dimensie in die DIO diere aangetoon (p<0.05). Tesame hiermee het die breedte van kardiomiosiete van die DIO diere toegeneem (p<0.0001) en daar was ook ‘n peri-nukluêre lokalisering van NFATc3. Behandeling van kontrole diere met ‘n GSK-3 inhibitor het insulienweerstandigheid ontlok soos afgelei uit ‘n verhoging in liggaamsgewig (p<0.05), serum insulien-vlakke (p<0.01) en die HOMA-IR waarde (p<0.01). In teenstelling het behandeling van die DIO diere met die GSK-3 inhibitor tot ‘n verbetering van insulienweerstandigheid gelei aangesien ‘n verlaging in serum insulien konsentrasies gevind is (p<0.05). Kardiomiosiete vanaf die behandelde DIO diere het ook ‘n verhoogde insulien-gestimuleerde glukose opname met 100nM insulien getoon (p<0.05). Behandeling met die GSK-3 inhibitor het die ontwikkeling van miokardiale hipertrofie in die kontrole diere teweeggebring, soos aangetoon deur ‘n toename in die ventrikulêre gewig (p<0.05) en ‘n groter selwydte in kardiomiosiete terwyl dit geen invloed op die bestaande hipertrofie van die vet diere gehad het nie. Gevolgtrekking: Die huidige studie het getoon dat die betrokke dieet asook behandeling met ‘n GSK-3 inhibitor insulienweerstandigheid sowel as die ontwikkelling van miokardiale hipertrofie in rotte ontlok. In die DIO diere het die behandeling met die GSK-3 inhibitor bloedglukose en insulien-vlakke verlaag en het nie hipertrofie vererger nie.

published_or_final_version / abstract / Anaesthesiology / Master / Master of Philosophy

<p>Myocardial infarction (MI) is often caused by a disruption of an atherosclerotic plaque with activation of coagulation, platelets and inflammation. The aims were; to investigate whether the oral direct thrombin inhibitor, ximelagatran affected markers for coagulation, platelet and inflammation in a patient cohort with recent MI and if the coagulation markers could identify patients with increased risk of new ischemic events; to evaluate some of the mechanisms involved in formation of platelet-monocyte aggregates (PMAs). </p><p>In a biomarker substudy patients with recent MI were randomized to 24-60 mg of ximelagatran or placebo for six months. There was a persistent dose-independent reduction of coagulation markers (F1+2, D-dimer) by ximelagatran treatment. 60 % reduced their D-dimer levels after one week and that group had less ischemic events during treatment. There was an early increase of the platelet activation marker and ximelagatran in higher doses attenuated these increased levels. Both in vivo and in vitro the direct thrombin inhibitor diminished procoagulant activity and tissue factor (TF) presenting microparticles. In contrast, the inflammatory markers increased after six months of ximelagatran treatment. The PMA-levels were elevated for long-term after MI. In vitro thrombin inhibition diminished formation of PMAs. Formation of PMAs in stimulated whole blood was P-selectin dependent and induced TF expression through phosphorylation of the Src-family member Lyn in monocytes.</p><p>Addition of an oral direct thrombin inhibitor reduces coagulation and platelet activation markers for long-term after a MI together with reduced procoagulant activity which may contribute to the clinical benefit of the drug. Early reduction of D-dimer levels seems to be suitable to identify patients with reduced risk of new ischemic events independent of antithrombotic treatment. Circulating PMAs persist after a MI connecting coagulation to inflammation. Within these aggregates P-selectin induces TF, the main initiator of coagulation, partly through phosphorylation of Lyn.</p>

<p>Vetskapen om att hjärtinfarkt till stor del kan förebyggas genom en hjärtskyddande livsstil gör området mycket intressant.</p><p><strong>Syfte:</strong> Att göra en undersökning över tid angående livsstilskunskap och beteende hos patienter som haft hjärtinfarkt med fokus på fysisk aktivitet, stresspåverkan, intag av frukt och grönsaker, samt rökning.</p><p><strong>Metod:</strong> Enkätutskick gjordes till två patientgrupper, som haft hjärtinfarkt för 2-4 månader sen (grupp 1, n = 35) respektive för ca 2 år sedan (grupp 2, n = 32). Svarsfrekvensen uppgick till 83 %. </p><p><strong>Resultat:</strong> Kunskapsmässigt framgick det att båda grupperna hade överlägset bäst kunskaper gällande rökning och stress. Störst osäkerhet rådde inom området frukt/grönsaker. Efter två år såg man att samtliga områden hade minskat i sin betydelse, dock marginellt inom fysisk aktivitet. Ett relativt gott hjärtskyddande beteende kan konstateras i patientgrupperna inom samtliga områden förutom stresshantering, vilket skilde sig markant från de övriga. En förändring till något sämre beteende över tid såg man inom rökning och marginellt rörande fysisk aktivitet. Gällande intag av frukt och grönt hade förändring skett både till det sämre och till det bättre. En förändring till ett bättre beteende sågs dock beträffande stresshanteringen. Beträffande hur kunskap stämde överens med beteende ses samma mönster för båda grupperna, d v s att det inom rökningen är bäst överensstämmelse, följt av fysisk aktivitet, intag av frukt och grönt, samt sist området stress. En minskning angående överensstämmande kan konstateras i grupp 2 i följande ordning, frukt/grönsaker, fysisk aktivitet och sist rökning. Inom stressområdet ökade istället överensstämmandet mellan kunskap och beteende över tid.</p><p><strong>Slutsats:</strong> Denna kartläggning antyder att koronarpatienters kunskaper och beteende är relativt tillfredsställande på kort och lång sikt, men kunskapsmässigt är det främst inom området frukt/grönsaker det finns utrymme för ytterligare förbättringar och beteendemässigt inom stresshantering, vilket bör främjas genom större vårdinsatser inom respektive område. </p>

No description available.

Cell-based therapies involving adipose-derived stem cells (ASCs) have shown promise in stimulating cardiovascular regeneration, including in the treatment of myocardial infarction (MI) and ischemic heart disease. However, previous studies involving the delivery of ASCs following MI have indicated that therapeutic efficacy has been limited by low survival and/or poor retention of the transplanted cells at the site of injury. To address these limitations, the goal of this thesis was to develop a more effective delivery strategy incorporating an injectable biomaterial combined with chemotactic growth factor delivery to enhance ASC retention within the gel. Working towards future in vivo analysis in a rat model, multilineage characterization studies confirmed that ASCs isolated from the epididymal fat pad of male Wistar rats could differentiate in vitro along the adipogenic, osteogenic, and chondrogenic lineages. Subsequently, the chemotactic response of the rat ASCs (rASCs) to varying concentrations of stromal derived factor-1 α (SDF-1α) and hepatocyte growth factor (HGF) was analyzed using a modified Boyden chamber assay. The results demonstrated that SDF-1α and HGF, at 20, 50, and 100 ng/mL elicited significant migratory responses under normoxic (21%) and hypoxic (5%) culture conditions. RT-PCR analysis was conducted to assess the expression of the two chemotactic growth factors and their associated receptors in the rASCs, and secreted SDF-1α protein expression was quantified by ELISA. Moving towards the development of the biomaterials-based delivery approach, the viability of rASCs encapsulated by photopolymerization in methacrylated glycol chitosan (MGC) hydrogels modified with various degrees of arginine-glycine-aspartic acid (RGD)-peptide modification was examined. More specifically, rASCs were encapsulated in MGC hydrogels with 0%, 4%, and 7% RGD modification and cultured for up to 14 days. Viability staining results indicated that rASC viability was enhanced in the 4% and 7% RGD-modified MGC hydrogels in comparison to the MGC hydrogels with no peptide modification. Pre-loading the gels with 50 ng/mL of SDF-1α had no significant effects on cell viability over 14 days. Overall, the results demonstrate that peptide modification to promote cell adhesion within the MGC hydrogels is key to improving cell viability and thereby improving the therapeutic potential of ASCs. / Thesis (Master, Chemical Engineering) -- Queen's University, 2012-10-24 23:54:37.126