Background: Current research has demonstrated that aspirin and fish oil (EFA) increase plasma levels of specialized pro-resolution molecules (SPMs). This study investigates their effects on SPM precursor pools in platelet rich fibrin (PRF). Methods: Twenty healthy volunteers were randomly assigned to take aspirin; EFA or aspirin and EFA. Four hours later, SPM precursor levels were quantified using combined Liquid Chromatography tandem mass spectrometry. The differences between the groups: Aspirin (yes or no), EFA (yes or no), were analyzed by ANCOVA, testing for group differences after covarying out the baseline value. Results: There were 4 significant interactions, 1 with an aspirin effect, 2 with an EFA effect, and 64 with no difference between the groups. The significant interaction effect was found for the following lipidome: LPE(20:4), LPI(16:1), LPI(18:1), and LPI(20:3). Aspirin decreased the LPG(16:4) levels, and EFA decreased the LPE(22:5) and PG(16:0/18:0) lipidomes. Conclusions: Some SPM precursor pools in PRF were increased following supplementation.

Background: The Framingham Study from 1991 showed a clear correlation between atrial fibrillation (AF) and ischemic stroke, where patients with AF had an almost fivefold increase in risk of stroke compared with patients without AF. Since then, several trials have evaluated different antithrombotic treatments to reduce the risk of stroke in patients with AF. Other trials have investigated factors that increase the risk of stroke in patients with AF and risk score systems have been developed to categorize patients into low or increased risk of stroke to help clinicians to decide which patients benefit from antithrombotic treatment and in whom it can be abstained, not to expose patients with low stroke risk to an increased risk of bleeding conferred by antithrombotic treatment. The aims of this thesis were: [1] to evaluate if a warfarin dosing algorithm can increase hit rate and decrease mean error compared with manually changed doses; [2] to assess the prevalence and net clinical benefit of aspirin as monotherapy for stroke prevention in AF; [3] to investigate the risk of thromboembolic and haemorrhagic complications within 30 days after electrical cardioversion (ECV) of AF in patients with and without oral anticoagulation (OAC) pre-treatment; and [4] to assess the proportion of patients discontinuing OAC after pulmonary vein isolation (PVI), identify factors predicting stroke after PVI and to investigate risk of complications after PVI with and without OAC. Materials and methods: All studies are retrospective and based on data from Swedish national quality registries. In paper I, data from Auricula was used to compare the resulting INR values after algorithmic warfarin dose suggestions and manually changed doses. In paper II data was extracted from the Swedish National Patient Register, the Dispensed Drugs Register and the Cause of Death Register. Patients with aspirin treatment were compared with patients without any antithrombotic treatment regarding risk of thromboembolic and haemorrhagic complications. In paper III data was collected from the Swedish National Patient Register and the Dispensed Drugs Register to examine risk of complications (thromboembolic and haemorrhagic events) within 30 days after cardioversion, comparing patients with and without oral anticoagulation pre-treatment. In paper IV data from six different Swedish national quality registries were used (Swedish Catheter Ablation Register, Auricula, Swedish National Patient Register, Dispensed Drugs Register, Cause of Death Register and Riksstroke). Patients undergoing pulmonary vein isolation (PVI) were investigated for adherence to guidelines regarding oral anticoagulation, predictors for stroke after PVI, as well as risk of ischemic stroke or intracranial haemorrhage after PVI in patients with and without treatment. Results: Paper I showed that a computerized dosing algorithm for warfarin in most cases perform as well or better compared with doses that have been changed manually, with a better hit-rate (0.72 vs. 0.67) and a lower mean error (0.44 vs. 0.48). Paper II showed that 32% of 182.678 patients with a diagnosis of AF were on monotherapy with aspirin for stroke prevention. A total of 115.185 patients were included, 58.671 with aspirin treatment and 56.514 without antithrombotic treatment at baseline. After stratification after CHA2DS2-VASc score and after multivariable adjustment, aspirin treatment did not confer a decrease in thromboembolic events. After propensity score mathcing, rate of ischemic stroke was 7.4%/year (95% CI 7.1-7.6) in aspirin treated patients and 6.6%/year (95% CI 6.4-6.9) in patients without antithrombotic treatment. In paper III 22.874 patients undergoing electrical cardioversion were included, 10.722 with and 12.152 without OAC pre-treatment. In patients with low stroke risk (CHA2DS2-VASc 0-1), no thromboembolic complication was seen within 30 days after cardioversion. In patients with CHA2DS2-VASc ≥2, the risk of thromboembolic complications was increased when no oral anticoagulation pre-treatment was used, results that remained after propensity score matching. No difference regarding haemorrhagic complications was seen. Paper IV included a total of 1585 patients undergoing PVI with a mean follow up of 2.6 years. Adherence to current guidelines regarding oral anticoagulation was good in patients with CHA2DS2-VASc ≥2. Previous ischemic stroke was a predictor for a new stroke after PVI. In patients with CHA2DS2-VASc ≥2 stroke risk was increased in patients discontinuing OAC compared to those continuing OAC (1,60%/year vs. 0.34%/year). Conclusion: Oral anticoagulation is still underutilized for prevention of stroke and systemic embolism in patients with atrial fibrillation. Patients with risk factors for stroke (CHA2DS2-VASc ≥2p) benefit from continuous oral anticoagulation treatment to prevent stroke, also in conjunction with electrical cardioversion and after pulmonary vein isolation. If warfarin is chosen, a computerised dosing algorithm can facilitate and standardize warfarin dosing and lead to better resulting INR values than manually changed doses. Aspirin should not be used for stroke prevention in patients with atrial fibrillation.

La tétraploïdie – cellule contenant le double du génome d’une cellule diploïde – est considérée comme un état métastable, à l’origine de l’aneuploïdie des cancers. Présentes dans les lésions précancéreuses, les cellules tétraploïdes sont associées à la progression tumorale. Etant donné le rôle clé de la tétraploïdie au cours de l’oncogenèse, le développement d’agents pharmacologiques éliminant spécifiquement les cellules tétraploïdes pourrait permettre de prévenir et limiter l’évolution vers un état cancéreux. Afin d'identifier des composés délétères pour les cellules tétraploïdes, nous avons développé une méthode de criblage basée sur la vidéomicroscopie à fluorescence automatisée. La chimiothèque de l'Institute of Chemistry and Cell Biology (ICCB) a été criblée, et nous avons mis en évidence plusieurs hits aux effets cytostatiques et/ou cytotoxiques préférentiels pour les cellules tétraploïdes. En raison de ses propriétés chimiopréventives, le resvératrol est le premier composé dont nous avons choisi de poursuivre la caractérisation. Sa sélectivité pour les cellules tétraploïdes a été confirmée sur différents types cellulaires, stables ou en cours de polyploïdisation. L’étude du mécanisme d’action anti-tétraploïde du resvératrol a permis d’identifier le senseur de la charge énergétique 5’-adenosine monophosphate-activated kinase (AMPK), comme une cible moléculaire responsable de la mort sélective des cellules tétraploïdes. Une série d’agents pharmacologiques activant directement ou indirectement AMPK – parmi lesquels l’aspirine et son métabolite le salicylate, dont l’action chimiopréventive a été établie par plusieurs études épidémiologiques et essais cliniques – a montré une toxicité préférentielle pour les cellules tétraploïdes. De la même manière que le resvératrol, ces agents éliminent les cellules tétraploïdes stables et limitent la polyploïdisation. Finalement, l’effet anti-tétraploïde du resvératrol et de l’aspirine a été évalué in vivo. L’administration orale de ces deux composés aux doses décrites comme chimiopréventives, réduit le développement des cellules épithéliales tétraploïdes et aneuploïdes des cryptes intestinales des souris ApcMin/+, le modèle murin de la polypose adénomateuse familiale. Collectivement les résultats de cette étude suggèrent que l’action chimiopréventive du resvératrol et de l’aspirine est associée à l’élimination des cellules tétraploïdes précurseur de tumeurs. / Tetraploidy – cells that contain twice the normal amount of chromosomes – is a metastable state leading to aneuploidy in cancer. Tetraploid cells have been observed in precancerous lesions and constitute a step toward tumor progression. Given the importance of tetraploidization for oncogenesis, developing drugs that selectively target tetraploid cells should prevent cancer.To discover compounds toxic to tetraploid cells, we developed an assay-system based on automatic fluorescence videomicroscopy. We screened the Institute of Chemistry and Cell Biology (ICCB) chemical library and identified several hits exerting a selective cytostatic and/or cytotoxic effect on tetraploid cells. Due to its well known chemopreventive properties, resveratrol was the first compound we further characterized. Its selectivity for tetraploid cells was confirmed on various stable or polyploidizing cancer cell lines, as well as primary epithelial cells. The mechanism accounting for the preferential killing of tetraploid cells involves the 5’-adenosine monophosphate-activated kinase (AMPK) signaling pathway. A series of additional agents that stimulate AMPK – including aspirin and salicylate whose chemopreventive action have been established by several epidemiological studies and clinical trials – display a selective toxicity toward tetraploid cells. Similar to resveratrol, these drugs eliminate stable tetraploid cells and reduce polyploidization. Finally, we validated the anti-tetraploid effect of resveratrol and aspirin in vivo. Oral treatment with either of these two compounds at chemopreventive doses, repressed the accumulation of tetraploid and subsequently aneuploid intestinal epithelial cells from the crypts of the ApcMin/+ mouse model of familial adenomatous polyposis.Collectively, our results suggest that the chemopreventive action of resveratrol and aspirin involves the elimination of tetraploid cancer cell precursors.

L'aspirine est l'anti-plaquettaire le plus largement prescrit à la phase aiguë de l'accident vasculaire cérébral (AVC) ischémique. Cependant, la survenue de récidives, malgré cette prescription, est fréquente. La description de l'effet de l'aspirine sur l'activité plaquettaire durant cette phase n'a jamais été réalisée. Elle pourrait mettre en évidence une moindre réponse plaquettaire et aider à établir de nouvelles stratégies thérapeutiques. Cinquante patients, ont reçu par voie orale 300 mg d'aspirine, suite à un AVC ischémique. Ensuite, des prélèvements sanguins ont été réalisés : entre 2 et 3 heures (T1), entre 23 et 24 heures (T2) après la prise d'aspirine et, pour des patients déjà traités quotidiennement par une dose inférieure, avant la prise d'aspirine (T0). Les concentrations sériques de thromboxane (TX) B2 ont été mesurées, ainsi que les agrégations induites par l'acide arachidonique, par le collagène à la concentration de 2µg/L (Col2) et 20 µg/L (Col20). Afin de diminuer l'effet des variations de condition d'expérience, les résultats pour Col2 ont été rapportés à ceux pour Col20 (Col2/20). Tous les patients ont présenté une réponse à l?aspirine visible à T1 avec de plus, des concentrations de TXB2 abaissées en comparaison à T0. Il existe une récupération de l'activité plaquettaire à T2 comparée à T1, montrée par les concentrations de TXB2 et le rapport Col2/20. La dose orale de 300 mg d'aspirine, donnée à la phase aiguë de l'AVC, entraîne une inhibition plaquettaire, mais avec une récupération visible sur 24 heures. Pour les patients déjà traités quotidiennement par une dose inférieure, elle permet de compléter l'inhibition de la voie TXA2 dépendante / Aspirin is the most commonly used antiplatelet treatment during the acute phase of cerebral ischemic events. But, despite this protection, early ischemic recurrences are frequent, and considered as clinical failures of this therapy. We studied laboratory parameters of the first 300 mg oral dose of aspirin given, within 48 hours, after ischemic cerebral event. Fifty patients were included. For all patients, two blood sampling were performed, the first, during the third hour after aspirin intake (T1) and the second during the twenty-fourth hour (T2). For patients already treated with a daily dose of aspirin, a supplementary withdrawn was done before aspirin intake (T0). Platelet reactivity was studied on the basis of serum thromboxane (TX) B2 levels and light transmission aggregometry after stimulation of platelet-rich plasma by acid arachidonic and collagen 2µg/mL reported to results with collagen 20 µg/mL (ratio Col2/20). Inhibition of platelet activity was observed, at T1, for all patients. There is a significant increase of TXB2 values, and of relative values of the ratio Col2/20, at T2 as compared to T1. For already aspirin treated patients, there is a significant decrease of TXB2 levels at T1 as compared to T0. There is a platelet reactivity recovery within 24 hours, following the first 300 mg oral dose of aspirin, during the acute phase of a cerebral ischemic event, and demonstrated by TXB2 levels and ratio Col2/20. This fact would favour early ischemic recurrences. However, this dose is able to complete the inhibition of the TXA2 pathway for already aspirin treated patients

Introdução: A interação entre os anticoagulantes e a agregabilidade plaquetária é complexa. Dados laboratoriais prévios mostraram que a dabigatrana aumenta a excreção urinária de metabólito do tromboxano, indicando efeito de ativação de plaquetas. Posteriormente, dados do estudo RELY sugeriram que a dabigatrana 150mg poderia aumentar o risco de infarto do miocárdio em pacientes com fibrilação atrial. Objetivos: Comparar a influência da Dabigatrana e Enoxaparina na agregabilidade plaquetária. Métodos: Estudo prospectivo, intervencionista, realizado em pacientes com doença arterial coronariana (DAC) crônica em uso de aspirina em baixas doses. Os indivíduos foram inicialmente designados para dabigatrana 150mg, 2x/dia, por 5 dias, seguido por um período de washout de 30 dias e depois para exoxaparina 1mg/kg, 2x/dia, por um período adicional de 5 dias. Os testes de função plaquetária foram realizados no início e após cada fase de intervenção, usando agregometria de sangue total p (MEA) (objetivo primário), ELISA para determinação quantitativa de tromboxano B2 (TXB2), Verify Now Aspirin e testes de coagulação (objetivos secundários). Resultados: Em comparação com os valores basais, a dabigatrana aumentou a agregabilidade plaquetária avaliada pelo teste MEA-ASPI (+5U ± 24,1), enquanto a enoxaparina diminuiu a agregabilidade plaquetária (-6U ± 22,2), p=0,012 para a comparação entre os grupos ). O mesmo padrão foi observado usando o ensaio TXB2 (+2pg/mL para dabigatrana, -13pg/mL para enoxaparina, p = 0,011). Não houve diferenças significativas entre os dois grupos em relação aos demais testes. Individualmente, a enoxaparina diminuiu significativamente a agregabilidade plaquetária por TXB2 [33 (16,5 - 95)pg/mL vs. 20 (10-52) pg/mL, respectivamente, p = 0,026), mas não foram observadas diferenças significativas individuais com a dabigatrana em relação aos valores basais. Conclusões: Em relação à agregabilidade plaquetária, há um efeito oposto significativo da dabigatrana (aumento) em comparação com a enoxaparina (diminuição). Individualmente, foi observada uma diminuição significativa na agregabilidade plaquetária apenas com a enoxaparina, quando comparada com valores basais / Background: The interaction between anticoagulants and platelet aggregation is complex. Previous laboratory data have shown that dabigatran increases urinary thromboxane metabolite excretion, indicating platelet-activating effect. Thereafter, data from RELY trial suggested that dabigatran 150mg could enhance the risk of myocardial infarction in atrial fibrillation patients. Objectives: To compare the influence of Dabigatran and Enoxaparin on platelet aggregation. Methods: Prospective, interventional study conducted in chronic coronary artery disease (CAD) patients taking low-dose aspirin. Subjects were assigned initially to dabigatran 150mg bid for 5 days followed by a washout period of 30 days and then to exoxaparin 1mg/kg bid for an additional 5 days period. Platelet function tests were performed at baseline and after each intervention phase using multiple electrode aggregometry (MEA) (primary endpoint), ELISA for plasma quantitative determination of thromboxane B2, Verify Now Aspirin and coagulation tests as secondary endpoints. Results: In comparison with the baseline values, dabigatran increased platelet aggregation evaluated by MEAASPI test (+5U ± 24.1), whereas enoxaparin decreased platelet aggregation (- 6U± 22.2), p=0.012 for the comparison between the groups). The same pattern was observed using theTxB2 assay (+2pg/mL for dabigatran, -13pg/mL for enoxaparin, p=0.011). There were no significant differences between both groups regarding the VerifyNow Aspirin or the other platelet function and coagulation tests utilized. Individually, enoxaparin significantly decreased platelet aggregation by TXB2 [33 (16,5 - 95) pg/mL vs. 20 (10-52) pg/mL, respectivamente, p = 0.026) but no significant differences were observed with dabigatran when individually compared to baseline. Conclusions: Regarding platelet aggregation, there is a significant opposite effect of dabigatran (increase) in comparison with enoxaparin (decrease). Individually, a significant decrease in platelet aggrebability was observed with enoxaparin, but no significant differences were observed with dabigatran

Various recent studies have suggested that regular intake of some non-steroidal anti-inflammatory drugs (NSAIDs) have a preventative effect against several types of tumours including breast cancer. The term nanotechnology refers to technology in which one-billionth of a meter is used as a scale for chemical particle size. This work aims to study the effect of both ibuprofen and aspirin on DNA damage using peripheral blood lymphocytes from breast cancer patients and comparing the results with those from healthy females as a control using the Comet and micronucleus assays. Western blot analysis (WBA) was used to investigate the effect of these drugs on XRCC3 and p53 proteins, whereas QPCR was to evaluate this effect on p53, cox1 and cox2 genes. Two hundred fifty ng/ml of ibuprofen (NP and bulk) and 500 ng/ml of aspirin (NP and bulk) were used to treat the lymphocytes. Both aspirin and ibuprofen caused a reduction in DNA damage and micronucleus formation. Aspirin, both forms, showed a reduction in DNA damage in the Comet and micronucleus assays. Ibuprofen both forms, by contrast, showed a statistically significant reduction in micronucleus frequency in the micronucleus assay, while its preventative effect with the Comet assay was weak or insignificant. NPs of both agents were more effective than bulk sizes. Using the Comet repair assay, aspirin and ibuprofen nano form catalysed DNA repair to a greater extent than their bulk forms. Also, both sizes showed better repair with NSAIDs compared to samples repaired without NSAIDs. In WBA aspirin increased the expression of XRCC3 protein in healthy cells. However, both NSAIDs decreased that expression in cells from BC patients. Furthermore, aspirin increased p53 expression in BC patients lymphocytes. With the QPCR method, results of both aspirin forms increased the expression of the p53 gene in BC patient cells statistically significantly. Both drugs reduced cox1 expression in healthy volunteers and cancer patients lymphocytes. Moreover, cox2 reduction was only in lymphocytes from BC patients. The results of this work are consistent with the view that NSAIDs, particularly aspirin and ibuprofen, could have a promising role in cancer treatment including breast cancer.

Despite increasingly sophisticated perioperative management, cardiovascular complications continue to be major challenges for the clinician. As a growing number of elderly patients with known coronary artery disease (CAD) or with risk factors for CAD are undergoing non-cardiac surgery, cardiovascular complications will remain a significant clinical problem in the future. The overall objective of this thesis was to study the incidence of myocardial damage and perioperative adverse cardiac events, to determine predictors of poor outcome and to assess the effect of a medical intervention in patients at risk undergoing non-cardiac surgery. The studies in this thesis were conducted on a total of 952 patients undergoing non-cardiac surgery. Studies I and IV were multicenter studies; whereas the patients included in studies II and III underwent non-cardiac surgery at Linkoping University Hospital, Sweden. The correlation between postoperative myocardial damage and short- and long-term outcome were studied in 546 patients, aged 70 years or older undergoing non-cardiac surgery of at least 30 minutes duration. This study showed a close correlation between postoperative myocardial damage and poor short- as well as long-term outcome. Elevated Troponin T was a strong independent predictor of mortality within one year of surgery. In 186 patients with ASA physical status classification III or IV undergoing non-elective surgery, the incidence of myocardial damage was 33%. In this study preoperative myocardial damage was an independent predictor of major adverse cardiac events in the postoperative period. In 69 patients with ASA physical status classification III & IV undergoing acute hip surgery, we found a close correlation between elevated NT-proBNP value prior to surgery and cardiac complications in the postoperative period. To study the effect of acetylsalicylic acid on postoperative myocardial damage and cardiovascular events, 220 patients at risk were randomized to receive 75 mg of acetylsalicylic acid or placebo 7 days prior to surgery until the third postoperative day. This study showed that treatment with acetylsalicylic acid resulted in an 8% (95% CI 1-15%) absolute risk reduction of having a postoperative major adverse cardiac event. No statistically significant differences of bleeding complications were seen between the groups. In conclusion, this thesis contributes to the understanding of the clinical relevance of elevated cardiac markers (with or without clinical or ECG signs of myocardial damage) in patients undergoing elective or emergency surgery. Moreover, we have identified predictors of poor outcome in the perioperative period that could be used as tools for identifying patients at risk. Finally, we have shown that continuing acetylsalicylic acid in the perioperative period reduced the risk of major adverse cardiac events within 30 days of surgery.

Abdominal aortic aneurysm (AAA) is a common disease that develops gradually over several years and is characterised by weakening and dilatation of the aortic wall. AAAs also demonstrates a marked inflammatory infiltrate throughout the aortic wall. Chlamydophila pneumoniae (C. pneumoniae), is a common bacterium. About 50% of the population has been infected in adolescence. Thirteen studies report the presence of either C. pneumoniae or its antigens in 35-100% of AAA specimens. The overall aim of this thesis was to evaluate the possible role of C. pneumoniae in inflammatory response and expansion of AAA from a clinical point of view. In paper I, viable C. pneumoniae was detected in a majority of 26 patients with AAA having open surgery. Patients operated for AAA had higher C. pneumoniae antibodies titers than controls. In paper II, 247 patients were randomised in a double-blind trial, to evaluate the effect of azithromycin on the expansion of small AAAs. No such effect was seen and there was no correlation between C. pneumoniae antibody titers and AAA expansion. In paper III, 42 patients with AAA were compared to 100 age- and sex matched controls with normal aortas. C. pneumoniae antibodies were analysed in plasma samples obtained at screening, and in samples from a study conducted 5-15 (mean 12) years previously on the same population. There was no significant difference between the groups. In paper IV, were 211 patients were analysed, we could not find an association between levels in plasma of three markers of inflammation (IL-6, MMP-9 and CRP) and AAA expansion. A significant reduction in AAA expansion rate was found in patients treated with a combination of ASA and statins. In conclusion, viable C. pneumoniae is found at the scene of the crime, but we were unable to reverse or halt expansion of AAA with antibiotic treatment. C. pneumoniae antibody titers cannot be used, to detect small AAA, or to evaluate AAA expansion. From a clinical point of view, based on the methods and analyses used in this thesis, the role of C. pneumoniae in the inflammatory response and expansion of abdominal aortic aneurysms is limited.

The thesis investigated nicotine levels and their effects on hypertensive subjects and whether aspirin could be used in the treatment of hypertension to bring about not only an anti thrombotic effect but reduce the systemic blood pressure especially in those individuals who smoke cigarettes. The study, which also audits the use of aspirin, was conducted in Kuwait and so provides an insight of hypertensive patients very rarely considered in the literature The thesis begins in Chapter One with an extensive literature review which analyses the properties and problems that nicotine causes and its ability to cause hypertensive changes along with its multitude of other events. The physiological and pathological problems caused by nicotine are reviewed on the basis of its chemistry and pharmacological properties using a worldwide perspective rather than just focus on Kuwait. The second Chapter uses extensive analysis of the literature to determine the pharmacological properties of aspirin and its use in cardiovascular disease. The pharmacokinetics and therapeutic effects are presented with emphasis to its inhibitory effects on platelet activation which is central to the development of serious cardiovascular consequences such as stroke and myocardial infarction. The third Chapter returns to consider the literature in detail and why nicotine has specific effects on the cardiovascular system in terms of receptor stimulation and how aspirin may be able to reduce nicotine's cardiovascular effects and concludes with the Aims and Objectives of the thesis. The fourth Chapter investigates urinary nicotine levels in smokers from cigarettes available in Kuwait to indicate the actual levels which could be achieved by smokers in this study. This established that the levels would cause pharmacological effects demonstrating also the effects of passive smoking. The number of cigarettes smoked per day has an unpredictable effect on metabolism and urinary output of nicotine. The fifth Chapter is the major investigational section of the thesis and considers if aspirin ability to reduce cardiovascular effects, may be useful in terms of diastolic blood pressure and lipid levels in the 4 blood. The effects were suggestive that aspirin did reduce the blood pressure in hypertensive subjects but was not universal and was limited to those suffering from mild - moderate hypertension. It was determined that aspirin should be sued at the earliest age possible in these patients. The sixth Chapter involved a large scale trial of the effectiveness of aspirin treatment in hypertensive patients over a one year period in Kuwait. This used ambulatory blood pressure measurements to determine the effectiveness of daytime and nightime changes in blood pressure in patients with and without aspirin treatment. The overall conclusion was a reduced relative risk of suffering cardiovascular events in mild to moderate hypertension when aspirin (75mg/day) was administered. Specifically in smokers, aspirin lowers the systolic daytime BP and diastolic nightime BP. To support this work a comprehensive audit is provided of the use of the current use of aspirin in Kuwait hospitals.

M. Tech. Engineering: Chemical. / Focuses on the emerging application of clinoptilolite in removing aspirin and cephalexin from municipal wastewater streams. The mechanisms of sorbent-organic compounds interaction was studied in detail. Specifically, this research aims to achieve the following objectives: I. to investigate the sorption capacity of surfactant modified clinoptilolite on the removal of aspirin and cephalexin ; II. To relate sorbents performance to process variables with sorbent properties and water quality ; III. to compare the sorption capacity of surfactant modified clinoptilolite to commercial emerging adsorbents on the removal of aspirin and cephalexin from aqueous solution ; IV. to apply existing mathematical models to describe isotherms and kinetic data in order to extract design parameters.