New Approach of Estimating Sarcasm Based on the Percentage of Happiness of Facial Expression Using Fuzzy Inference System

The procedure of determining whether micro expressions are present is accorded a high priority in the majority of settings. This is due to the fact that despite the best attempts of the person, these expressions will always expose the genuine sentiments that are buried under the surface. The purpose of this study is to provide a novel approach to the problem of measuring sarcasm by using a fuzzy inference system. The method involves analysing a person's facial expressions to evaluate the degree to which they are taking pleasure in something. It is feasible to distinguish five separate areas of a person's face, and precise active distances may be determined from the outline points of each of these regions. This category includes the brows on both sides of the face, as well as the eyes and lips. In order to arrive at a representation of an individual's degree of happiness while working within the parameters of the fuzzy inference system that has been provided, membership functions are first applied to computed distances. After that, the findings from the membership functions are put to use in yet another membership function so that an estimate of the sarcasm percentage may be derived from them. The suggested method is validated by using photos of human faces taken from the SMIC, SAMM, and CAS(ME) 2 datasets, which are the industry standards. This helps to guarantee that the method is effective

T2 and T2⁎ mapping and weighted imaging in cardiac MRI

Cardiac imaging is progressing from simple imaging of heart structure and function to techniques visualizing and measuring underlying tissue biological changes that can potentially define disease and therapeutic options. These techniques exploit underlying tissue magnetic relaxation times: T1, T2 and T2*. Initial weighting methods showed myocardial heterogeneity, detecting regional disease. Current methods are now fully quantitative generating intuitive color maps that do not only expose regionality, but also diffuse changes – meaning that between-scan comparisons can be made to define disease (compared to normal) and to monitor interval change (compared to old scans). T1 is now familiar and used clinically in multiple scenarios, yet some technical challenges remain. T2 is elevated with increased tissue water – edema. Should there also be blood troponin elevation, this edema likely reflects inflammation, a key biological process. T2* falls in the presence of magnetic/paramagnetic materials – practically, this means it measures tissue iron, either after myocardial hemorrhage or in myocardial iron overload. This review discusses how T2 and T2⁎ imaging work (underlying physics, innovations, dependencies, performance), current and emerging use cases, quality assurance processes for global delivery and future research directions

Molecular imaging of tissue repair after myocardial infarction : preclinical evaluation of novel 68Ga-labeled PET tracers

Congestive heart failure (HF) develops soon after acute myocardial infarction (AMI) in almost 25% of initial survivors. Modern cardiac imaging methods are useful for HF diagnostics and, possibly, the detection of underlying molecular mechanisms involved in myocardial repair. CD44, a cell-surface glycoprotein, is involved in various cellular functions, including cell proliferation, adhesion, migration and lymphocyte activation. Integrins are transmembrane proteins involved in various signaling pathways related to inflammation, angiogenesis and fibrosis. Expression of proteolytic matrix metalloproteinases 2 and 9 (MMP-2/9) also associates with extracellular matrix remodeling. The purpose of this thesis was to evaluate novel Gallium-68 labeled imaging agents targeting αvβ3 integrin, MMP-2/9, or CD44, for positron emission tomography (PET) imaging of post-MI repair in a surgical rat model. The MMP- 2/9 targeting tracer watarkias also evaluated for imaging of atherosclerotic lesions in a hypercholesterolemic mouse model. In vivo PET imaging, ex vivo biodistribution, ex vivo autoradiography, and immunohistochemistry were utilized to assess tracer stability, uptake in various tissues, as well as uptake correlation with various cellular level processes. Of the studied tracers, αvβ3 integrin targeting tracer showed the most optimal characteristics for imaging of myocardial healing processes. Tracer uptake in the damaged myocardium was clearly visible in vivo, and blood clearance as well as tracer stability were sufficient. The CD44 targeting tracer showed initial potential warranting further development, as the tracer uptake was associated with myocardial inflammation. MMP-2/9 targeted imaging showed significant limitations due to tracer instability and slow clearance. In conclusion, imaging of αvβ3 integrin expression is a potential tool for the purpose of evaluating myocardial repair after MI.Sydänkudoksen infarktinjälkeisen paranemisen molekyylikuvantaminen : uusien 68Ga-leimattujen merkkiaineiden prekliininen arviointi Sydämen vajaatoiminta kehittyy pian akuutin sydäninfarktin jälkeen lähes 25 prosentille eloonjääneistä. Nykyaikaiset sydämen kuvantamismenetelmät ovat hyödyllisiä diagnostiikassa ja mahdollisesti sydänlihaksen muovautumiseen liittyvien molekyylimekanismien havaitsemisessa. Solupinnan glykoproteiini CD44 osallistuu erilaisiin soluvälitteisiin toimintoihin, kuten proliferaatioon, adheesioon, migraatioon ja lymfosyyttien aktivaatioon. Integriinit ovat transmembraaniproteiineja, jotka osallistuvat erilaisiin signalointireitteihin liittyen tulehdukseen, angiogeneesiin ja fibroosiin. Proteolyyttisten matriksin metalloproteinaasi 2:n ja 9:n (MMP-2/9) ilmentyminen liittyy niin ikään solunulkoisen matriksin uudelleenmuovautumiseen. Tämän väitöskirjan tarkoituksena on arvioida uusia Gallium-68-leimattuja koettimia positroniemissiotomografiaa (PET) varten. Tutkitut koettimet kohdistuvat joko αvβ3-integriiniin, MMP-2/9:ään tai CD44:ään. Tutkimus toteutettiin infarktinjälkeisen sydämen vajaatoiminnan kirurgisessa rottamallissa. MMP-2/9-koetinta arvioitiin myös ateroskleroottisten muutosten kuvantamiseen hyperkolesterolemisessa hiirimallissa. αvβ3-integriiniin kohdentuvan merkkiaineen kertymä näkyi selkeästi in vivo, ja veren puhdistuma sekä merkkiaineen stabiilisuus olivat riittävät. CD44 kuvantamiskohteena osoitti alkuvaiheen potentiaalia, joka mahdollistaa jatkokehityksen, sillä merkkiaineen kertymä assosioitui infarktinjälkeiseen tulehdusreaktioon. MMP-2/9- kohdennetulle kuvantamiselle puolestaan ilmeni merkittäviä rajoituksia merkkiaineiden epävakauden ja hitaan veripuhdistuman vuoksi Yhteenvetona voidaan todeta, että αvβ3-integriinifragmentin kuvantaminen on potentiaalinen työkalu sydänlihaksen paranemisprosessien arvioimiseksi akuutin sydäninfarktin jälkeen

STUDIES INTO THE MECHANISMS UNDERLYING THE CARDIAC ANTI- HYPERTROPHIC AND ANTI-REMODELLING EFFECTS OF GINSENG

Ginseng is a widely prescribed herbal drug that has been used for over 2000 years in Asia for the treatment of several different disorders of the body including those of the cardiovascular system. Advances in ginseng research have identified the bioactive constituents considered responsible for eliciting its pharmacological effects known as ‘ginsenosides’. Several published reports have demonstrated the potential ability of ginseng and their isolated ginsenosides in the prevention and treatment of heart disease. In the study presented here the effects of ginseng on agonist-induced cardiac hypertrophy in isolated cardiomyocytes (Chapter 2 - 4) as well as an in vivo model of heart failure (Chapter 4) were investigated. In our first study (Chapter 2), the ability of ginseng to prevent leptin-induced ventricular cardiac hypertrophy by inhibiting pi 15RhoGEF-RhoA/ROCK-dependent MAPK activation was investigated. Leptin (50 ng/ml, which is a concentration representative of plasma levels found in obese individuals) produced a robust hypertrophic response that was associated with RhoA/ROCK activation resulting in a significant increase in cofilin-2 phosphorylation and actin polymerization, the latter evidenced by a reduction in the globular to filamentous actin ratio. These effects were prevented by North American ginseng (alcoholic extract; 10 pg/ml), hereon referred to as “ginseng”. The stimulation of RhoA/ROCK by leptin was associated with significantly increased pll5RhoGEF gene and protein expression and exchange activity, all of which were inhibited by ginseng. The attenuation of leptin-induced activation of RhoA/ROCK by ginseng was further associated with diminished p38 MAPK activation and nuclear translocation. In a follow-up study (Chapter 3), the ability of ginseng to reverse leptin-induced cardiac hypertrophy by enhancing Rnd3-pl90RhoGAP-mediated downregulation of RhoA/ROCK activation, was investigated. Cardiomyocytes incubated with leptin for 48 h displayed significantly increased cell surface area, which was accompanied by an increase in the expression of the fetal gene a-skeletal actin. A decrease in the G/F actin ratio, most likely as a result of RhoA/ROCK cofilin-2 phosphorylation was observed in hypertrophied cells treated with leptin. Treatment with ginseng however reversed these effects. In leptin-treated cells, Rnd3 gene and protein expression were decreased however treatment with ginseng reversed these effects by leptin. In the left ventricular tissues of rats subjected to four weeks of sustained myocardial infarction (MI), Rnd3 protein expression was markedly reduced while p63RhoGEF and ROCK expressions, which reflect upregulation of RhoA, were increased. These Mi-induced effects however were restored by ginseng to expressions as observed in sham. For our third study (Chapter 4), we investigated the ability of ginseng to reverse already established cardiac dysfunction as well as hypertrophy both in vitro and in vivo by inhibition of calcineurin/NFAT3 activation. The ability of a pharmacological agent to reverse HF is of particular importance as the majority of current treatments are unable to reverse already established myocardial remodelling and ventricular dysfunction. Accordingly, ginseng was administered in drinking water ad libitum to rats after 4 weeks of sustained coronary artery ligation (CAL) when hypertrophy and HF were established or to hypertrophic neonatal ventricular myocytes treated with angiotensin II, endothelin-1 or phenylephrine. Echocardiographie and catheter-based measurements of hemodynamic parameters revealed complete reversibility of systolic and diastolic abnormalities as well as increased myocardial collagen gene expression in CAL-rats after treatment with ginseng. Similarly, ginseng administration to hypertrophic cardiomyocytes resulted in complete reversal to a normal phenotype after 24 h as determined by cell surface area and a-skeletal gene expression. The IV effects of ginseng in vivo were associated with a tendency to attenuate calcineurin activation and MCIP-1 gene expression. In the cultured cardiomyocytes however, ginseng completely reversed agonist-induced calcineurin activation and NFAT3 nuclear translocation. Taken together, results from our studies demonstrate a marked anti-hypertrophic and anti-remodelling ability of ginseng in the prevention and treatment of cardiovascular diseas

Characterising haemodialysis-associated cardiomyopathy using deformation imaging by cardiovascular magnetic resonance tagging and speckle-tracking echocardiography

Haemodialysis patients represent an extreme phenotype of cardiovascular risk with a pattern of disease distinct from that in the general population. Non-traditional risk factors, specific to chronic kidney disease such as hypervolaemia, arterial stiffness and advanced glycation end-product deposition are increasingly recognised. A previously demonstrated non-traditional risk factor associated with worse outcomes is the presence of uraemic cardiomyopathy. This pattern of cardiac morphology and function has previously been defined as the presence of left ventricular abnormalities, including left ventricular hypertrophy, dilatation and left ventricular systolic dysfunction. For the first time the work in this thesis studies an incident haemodialysis population using multi-parametric strain-based imaging. This uses the accuracy of cardiovascular magnetic resonance imaging of resting cardiac and aortic morphology and function augmented with strain by tagging to longitudinal strain changes during haemodialysis by speckle-tracking echocardiography. The general aim of this thesis was to characterise the relationship of left ventricular function to haemodialysis using strain-based imaging. This might allow characterisation of haemodialysis-associated cardiomyopathy which may be distinct from the traditional definition of uraemic cardiomyopathy and may better define those patients who would benefit from modifications to the process of haemodialysis