Dissertations / Theses on the topic 'Statin'
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Schick, Brian Adam. "Statin-induced muscle mitochondrial toxicity." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/908.
Full textSiddiqui, Moneeza Kalhan. "Genetic factors in statin intolerance." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/5852fdf4-5737-4c23-a391-f0bc4e627ebb.
Full textWong, Ho-kwan Hogan, and 黃浩權. "A church and community centre, Statin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31982608.
Full textMack, Deborah Sara. "Statin Pharmacotherapy in U.S. Nursing Homes." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1104.
Full textWong, Ho-kwan Hogan. "A church and community centre, Statin." Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25945865.
Full textStringer, Henry. "Mitochondrial DNA alterations and statin-induced myopathy." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/9949.
Full textTimoney, Maire Christine. "Synthetic and biosynthetic approaches to statin analogues." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621819.
Full textLink, Emma. "Genome-wide association of statin-induced myopathy." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:ca675486-d678-4200-8bb4-988a923e9c4c.
Full textBoyle, Ashley Kathryn. "Effect of statin treatment on preterm labour." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29558.
Full textOstrowski, Stephen M. "Pleiotropic mechanisms of statin action in Alzheimer's Disease." Cleveland, Ohio : Case Western Reserve University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1190669698.
Full textTurner, R. "Statin-associated muscle toxicity : clinical and genomic perspectives." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3020572/.
Full textOstrowski, Stephen M. "Pleiotropic Mechanisms of Statin Action in Alzheimer's Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1190669698.
Full textPeterson, Mikael, and Matthew Martin. "Statin Medication Acquisition Among Medicare Beneficiaries 1992-2002." The University of Arizona, 2007. http://hdl.handle.net/10150/624409.
Full textObjectives: To investigate the relationship of price and prevalence of statins when new mediations enter the market and when old medications are withdrawn from the market. Methods: Patients that received a statin were enrolled in the Medicare Current Beneficiary Survey (MCBS) from 1992 to 2002. The overall prevalence of each statin as well as the prevalence of each statin for a patient’s drug coverage (no coverage, Medicaid, Medigap, employer coverage, or other public coverage) were analyzed. Results: The overall prevalence of statin was statistically significant for 1992 versus 2002 (p<0.001). When atorvastatin came to the market towards the end of 1996, there was no difference between simvastatin (p=0.24) and pravastatin (p=0.12) in 1997 versus 1998. Conclusions: There was a difference in the prevalence of statins when atorvastatin entered the market. When cerivastatin left the market, there was a difference in the prevalence of statin use. Atorvastatin became the most prevalent statin by the end of 2002. The price of statins appeared to decrease over time from $39.01 in 1992 to $31.95 in 2002. Also, the year atorvastatin was released the average price of statins increased to $36.57 in 1997.
Pietersen, Lauren. "Coenzyme Q10 for statin-induced myopathy : a systematic review." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/71937.
Full textENGLISH ABSTRACT: Background Statins are drugs of known efficacy in the treatment of hypercholesterolaemia. However, statin-induced myopathy, an adverse effect of statins in up to 15% of its users, has warranted a reduction in the prescription dose or discontinuation of the drug. The exact mechanism of statin-induced myopathy is unknown, but the potential of Coenzyme Q10 (CoQ10) as treatment has been recognized due to decreased human plasma CoQ10 levels found after statin use and the concomitant role of CoQ10 in muscle function. Objectives This systematic review assessed the effect of CoQ10 supplementation on: the severity of statin-induced myopathic symptoms, levels of plasma creatine kinase, intramuscular and plasma CoQ10, as well as whether any adverse effects of CoQ10 supplementation such as abdominal pain, nausea and vomiting or headaches were experienced. Search methods Two searches for studies were conducted in The Cochrane Central Register of Controlled Trials (inception to March 2011 and inception to November 2011), MEDLINE (inception to March 2011 and inception to November 2011), Web of Science (inception to March 2011 and inception to November 2011), Science Direct (inception to March 2011 and inception to February 2012), Wiley Online Library (inception to March 2011 and inception to February 2012), Springerlink (inception to April 2011 and inception to February 2012), EBSCOhost [Academic Search Premier and CAB abstracts (inception to March 2011 and inception to February 2012), CINAHL (inception to March 2011 and inception to November 2011)], Scopus (inception to March 2011 and inception to November 2011) and Google Scholar (inception to March 2011 and inception to February 2012). Reference lists of articles were hand searched for relevant clinical trials. Only trials with a full text were included in the review. Selection criteria Randomised controlled trials (RCTs) were included with adult participants (mean of 18-64.99 years) of all race/ethnic groups and gender on statin therapy with reported myopathic symptoms from an unknown cause. The intervention was in the form of a pure oral supplement of CoQ10 irrespective of dose, duration and frequency, and the control in the form of a placebo, a similar antioxidant, or no intervention. Outcomes included the severity of myopathic symptoms, levels of plasma creatine kinase (U/L), intramuscular CoQ10 (μmol/kg) and plasma CoQ10 (μmol/L), as well as adverse effects of CoQ10. Data collection and analysis The principle investigator and one independent reviewer selected the studies, extracted data and assessed for risk of bias using the Cochrane Collaboration‘s tool for assessing risk of bias. Authors of relevant clinical trials were contacted for additional information. Results Two RCTs were included in the review, totaling 76 participants. A meta-analysis could not be performed, thus the review is narrative. There were an insufficient number of RCTs to confirm whether routine supplementation of CoQ10 improves statin-induced myopathic symptoms. Conclusions More and larger RCTs are required to determine the efficacy of CoQ10 supplementation in statin-induced myopathy. Consensus needs to be reached regarding the definition and measurement instrument/s of myopathy so that results of future studies can easily be compared and synthesized.
AFRIKAANSE OPSOMMING: Agtergrond Statiene is medikasie bekend vir die effektiewe behandeling van hipercholesterolemie. Statien-geïnduseerde miopatie is egter 'n newe-effek wat voorkom in tot 15% van gebruikers, wat 'n vermindering in die voorgeskrewe dosis of staking van die medikasie tot gevolg het. Die presiese meganisme van statien-geïnduseerde miopatie is onbekend, maar die potensiaal van Koënsiem Q10 (CoQ10) is geïdentifiseer as 'n moontlike behandeling aangesien menslike plasma CoQ10 vlakke verlaag na die gebruik van statiene en as gevolg van die rol van CoQ10 in spierfunksie. Doelwitte Hierdie sistematiese literatuuroorsig het die effek van CoQ10 supplementasie bepaal op: die graad van statien-geïnduseerde miopatiese simptome, plasma kreatien kinase vlakke, intra-muskulêre en plasma CoQ10 vlakke, asook die teenwoordigheid van enige newe-effekte van CoQ10 supplementasie soos abdominale pyn, naarheid en braking of hoofpyne. Soektogstrategie Twee soektogte vir studies is uitgevoer in The Cochrane Central Register of Controlled Trials (ontstaan tot Maart 2011 en ontstaan tot November 2011), MEDLINE (ontstaan tot Maart 2011 en ontstaan tot November 2011), Web of Science (ontstaan tot Maart 2011 en ontstaan tot November 2011), Science Direct (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012), Wiley Online Library (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012), Springerlink (ontstaan tot April 2011 en ontstaan tot Februarie 2012), EBSCOhost [Academic Search Premier en CAB abstracts (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012), CINAHL (ontstaan tot Maart 2011 en ontstaan tot November 2011)], Scopus (ontstaan tot Maart 2011 en ontstaan tot November 2011) en Google Scholar (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012). Verwysingslyste van artikels is ook met die hand nagegaan vir relevante kliniese proewe. Slegs kliniese proewe waarvan die volteks beskikbaar was, is ingesluit in die oorsig. Seleksiekriteria Ewekansige gekontroleerde proewe (EGP) is ingesluit met volwasse deelnemers (gemiddeld 18-64.99 jaar) van alle rasse/etniese groepe en geslag op statien-terapie met gerapporteerde miopatie simptome van onbekende oorsaak. Die intervensie was 'n suiwer orale supplement van CoQ10 ongeag die dosis, duurte en frekwensie, en die kontrole 'n plasebo, soortgelyke antioksidant, of geen intervensie. Uitkomste het ingesluit: die graad van miopatie simptome, vlakke van plasma kreatien kinase (U/L), intra-muskulêre CoQ10 (μmol/kg) en plasma CoQ10 (μmol/L), sowel as newe-effekte van CoQ10. Dataversameling en -analise Die hoof ondersoeker en een onafhanklike hersiener het die seleksie van studies en data-ekstraksie onderneem en die risiko vir sydigheid geassesseer deur gebruik te maak van die Cochrane Collaboration’s tool for assessing risk of bias. Outeurs van relevante kliniese proewe is geraadpleeg vir addisionele inligting Resultate Twee EGP is ingesluit in die oorsig met 'n totaal van 76 deelnemers. 'n Meta-analise kon nie uitgevoer word nie, dus is die oorsig beskrywend. Daar was te min EGP om te bewys dat roetine supplementasie van CoQ10 statien-geïnduseerde miopatiese simptome verbeter. Gevolgtrekkings Meer en groter EGP is nodig om die effektiwiteit van CoQ10 supplementasie in statien-geïnduseerde miopatie te bepaal. Konsensus moet bereik word ten opsigte van die definisie en metingsinstrument/e van miopatie sodat die resultate van toekomstige studies makliker vergelyk en verwerk kan word.
Clark, Justin. "An evaluation of Warfarin and Statin Drug-Drug Interactions." The University of Arizona, 2012. http://hdl.handle.net/10150/623593.
Full textObjectives: To evaluate the literature with respect to drug-drug interactions of the hydroxymethylglutaryl CoA reductase inhibitors atorvastatin, fluvastatin, lovastatin, pitavastitin, pravastatin, simvastatin, and rosuvastatin with warfarin. Methods: This descriptive retrospective study identified articles reporting on each drug-drug interaction from the online databases PubMed (1970 – February 2012) and the drug compendia Micromedex and Facts & Comparisons. The studies included in this investigation were primary literature reports, written in English with human subjects. All studies included were evaluated using the van Roon 5-point quality of evidence scale developed in the Netherlands to assess drug-drug interactions. This scale rates the study type from lowest to highest quality, from zero to four. Case-reports were evaluated using the Drug Interaction Probability Scale (DIPS). The DIPS tool uses 10 questions to evaluate the probability that an adverse event is caused by a drug-drug interaction. Results: Twenty studies met the inclusion criteria. One study involved atorvastatin, four for fluvastatin, three for lovastatin, 2 for pitavastatin, 1 for pravastatin, 5 for rosuvastatin, and 6 for simvastatin. The mean van Roon quality of evidence score was 2.1+/- 0.74, the mean score for atorvastatin, pitavastatin, and pravastatin was 3, with the mean score of fluvastatin, lovastatin, rosuvastatin, and simvastatin was 2. 70% of the literature reviewed were case-reports or letters. Conclusions: The studies and reports supporting HMG-CoA reductase inhibitors and warfarin drug-drug interactions are most commonly case- reports and are of low quality and quantity.
Clark, Justin, and Daniel Malone. "An Evaluation of Warfarin and Statin Drug-Drug Interactions." The University of Arizona, 2012. http://hdl.handle.net/10150/614476.
Full textObjectives: To evaluate the literature with respect to drug-drug interactions of the hydroxymethylglutaryl CoA reductase inhibitors atorvastatin, fluvastatin, lovastatin, pitavastitin, pravastatin, simvastatin, and rosuvastatin with warfarin. Methods: This descriptive retrospective study identified articles reporting on each drug-drug interaction from the online databases PubMed (1970 – February 2012) and the drug compendia Micromedex and Facts & Comparisons. The studies included in this investigation were primary literature reports, written in English with human subjects. All studies included were evaluated using the van Roon 5-point quality of evidence scale developed in the Netherlands to assess drug-drug interactions. This scale rates the study type from lowest to highest quality, from zero to four. Case-reports were evaluated using the Drug Interaction Probability Scale (DIPS). The DIPS tool uses 10 questions to evaluate the probability that an adverse event is caused by a drug-drug interaction. Results: Twenty studies met the inclusion criteria. One study involved atorvastatin, four for fluvastatin, three for lovastatin, 2 for pitavastatin, 1 for pravastatin, 5 for rosuvastatin, and 6 for simvastatin. The mean van Roon quality of evidence score was 2.1+/- 0.74, the mean score for atorvastatin, pitavastatin, and pravastatin was 3, with the mean score of fluvastatin, lovastatin, rosuvastatin, and simvastatin was 2. 70% of the literature reviewed were case-reports or letters. Conclusions: The studies and reports supporting HMG-CoA reductase inhibitors and warfarin drug-drug interactions are most commonly case-reports and are of low quality and quantity.
Hannum, Cameron, Kevin Hawkins, Jenene Spencer, and Elizabeth Hall-Lipsy. "Grapefruit-Statin Interactions: Patient Awareness, Knowledge and Contributing Factors." The University of Arizona, 2016. http://hdl.handle.net/10150/613968.
Full textObjectives: The goals of this study were: to assess patients’ knowledge of grapefruit interactions when taking statin class (dyslipidemia) medications, to identify any pertinent demographic characteristics that may influence knowledge of grapefruit statin interactions, and to identify patient preferred sources of health information. Methods: Questionnaires were administered at community health fairs during the academic school year 2014 through 2015. The survey addressed grapefruit consumption, frequency and amount, for both whole fruit and juice; examined knowledge of the potential for harmful interactions of grapefruit juice with statin medications; and how or where the participant learned this information. Results: A total of 74 participants completed surveys, of which, 72 submitted fully completed surveys, mean age was 64 (SD=+/- 15.6), 71.2% were female (N=52), and 78.1% were white. Of those surveyed, 63.5% (N= 47) reported consuming grapefruit in the past 12 months, and 36.1% (N=26) reported taking a statin. Those taking statins, 50% (N=13) reported consuming grapefruit as well. The majority of people, 61.3% (N=45), reported obtaining health related information from healthcare sources. Those with a college education were more likely to have consumed grapefruit in the last 12 months (X2=4.88, p=0.027) and to have ever consumed grapefruit (X2 =4.40, p=0.036). Conclusions: The majority of the health fair attendees surveyed were highly educated, reported having health insurance, had consumed grapefruit in the past year, and had heard about grapefruit-drug interactions.
Kurniawan, Dede Indra. "Statin-induced myopathy and the benefit of oral administration of coenzyme Q10." Thesis, Curtin University, 2007. http://hdl.handle.net/20.500.11937/1014.
Full textKeskiväli-Bond, Piia. "Effects of acute early age statin treatment on rat vasculature." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/374917/.
Full textPiecha, Malgorzata Trebše Polonca. "Stability and degradation studies of cholesterol-lowering statin drugs : dissertation /." Nova Gorica : [M. Piecha], 2009. http://www.p-ng.si/~vanesa/doktorati/okolje/12Piecha.pdf.
Full textPrebreza, Nebih. "Statin-Therapie nach koronarer Stentimplantation und das Überleben nach einem Jahr." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96959870X.
Full textPasha, Rand. "The Role of Coenzyme Q10 in Statin Treated Zebrafish (Danio rerio)." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31427.
Full textMao, Pei-Lin. "Molecular characterization of statin, a protein marker for non-proliferating cells." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59812.
Full textLoughrey, Brona Veronica. "Effect of statin therapy on monocyte function in the metabolic syndrome." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534628.
Full textTaha, Dhiaa A. "Influence of acid-base imbalance and hyperlipidaemia on statin-induced myotoxicity." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40222/.
Full textNoal, D., R. L. Gauer, and Rick L. Wallace. "What Patients Without CAD or Equivalents Should be on a Statin?" Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/8691.
Full textAlsalman, Abdulkhaliq. "Impact of Statin Therapy on Outcomes in Aneurysmal Subarachnoid Hemorrhage Patients." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1994.
Full textZhao, Tong Tong. "Mechanism and Therapeutic Potential of Statin-Mediated Inhibition of Tyrosine Kinase Receptors." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20334.
Full textMushashi, Fidela. "Impact of British Columbia's reduction in generic drug prices on statin adherence." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/60125.
Full textMedicine, Faculty of
Graduate
Ooi, Esther M. M. "Regulation of lipoprotein transport in the metabolic syndrome : impact of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0125.
Full textBailey, Kristian M. "Cytochrome p450 variation and response to statin therapy following acute coronary syndrome." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578691.
Full textKilias, Antonios [Verfasser]. "Experimentelle Untersuchungen zu Wirkmechanismen der Statin-bedingten Modulation der Angiogenese / Antonios Kilias." Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1064096905/34.
Full textNoonan, Katherine. "Do anti-inflammatory agents promote linear ablation lesion discontinuities? : an electrophysiological examination." Thesis, Queensland University of Technology, 2011. https://eprints.qut.edu.au/49852/1/Katherine_Noonan_Thesis.pdf.
Full textBakar, Nur Salwani. "Investigation of the association between genetics, drug exposure and statin-induced muscle toxicity." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/3083.
Full textDonnelly, Louise. "Genetic and clinical determinants of lipid-lowering response to statin therapy in diabetes." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505632.
Full textAldujaily, Esraa Abdulaal. "An investigation of tumour-associated macrophages and statin therapy in human pulmonary adenocarcinoma." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/43086.
Full textKelley, Leslie K. "Effectiveness of Statin and Bisphosphonate Treatment in a 3NP model of Huntington’s Disease." ScholarWorks@UNO, 2015. http://scholarworks.uno.edu/td/1993.
Full textNelson, DeAnn Lynn, and DeAnn Lynn Nelson. "Promoting the Use of Statin Therapy in Navajo Patients with Type 2 Diabetes." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/625670.
Full textCoker, Joyce Feyisitan. "Statin-use and the adoption of healthy lifestyle choices : a cross-national comparison." Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/13195/.
Full textMorioka, Travis Y. "The association of serum 25-hydroxyvitamin D status and statin-associated musculoskeletal symptoms." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12534.
Full textObjectives: In this study, we investigated the relationship between serum vitamin D status and the prevalence of musculoskeletal pain among individuals on statin therapy. We hypothesized that lower serum vitamin D concentration would be associated with a higher odds of self-reported musculoskeletal pain among statin users. Background: HMG-CoA reductase inhibitors, or statins, are widely used lipid-lowering drugs that significantly reduce morbidity and mortality associated with heart disease. Statin use is associated with a higher prevalence of self-reported musculoskeletal pain in the general population. Non-blinded studies have shown improvement in statin-associated myalgia symptoms and increased tolerance to statin therapy after treatment of vitamin D deficiency. Methods: We performed secondary data analyses using the National Health and Nutrition Examination Survey (NHANES) 2001-2004. Employing SAS and SUDAAN, we carried out logistic regression to evaluate whether vitamin D deficiency modified the relationship between statin use and musculoskeletal pain. Based on a priori assumptions, we adjusted for the effects of demographics, selected disease states, and health habits in the logistic regression model. We also explored concentration-related trends of the effect of vitamin D on musculoskeletal pain. Results: Among 5941 participants age 40 years and older, the mean serum vitamin D concentration was 23.5 ng/mL [95% Confidence Interval (CI) 22.4, 24.2]. There was no significant difference in the mean serum vitamin D concentration between statin users (23.3 ng/mL, 95% CI 22.3, 24.3) and non-statin users (23.5 ng/mL, 95% CI 22.8, 24.2). Statin users had higher odds [adjusted odds ratio (aOR) 1.57, 95% CI 1.15, 2.13)] of self-reported musculoskeletal pain in any area (specifically including the lower extremities, lower back, upper extremities, and upper back) compared with non-users. Vitamin D deficiency was not a predictor of musculoskeletal pain (aOR 0.95, 95% CI 0.70, 1.28) in the overall sample. However, we found vitamin D deficiency to have a significant interaction with statin use for the outcome of musculoskeletal pain (p for interaction = 0.01). After stratifying the sample according to statin use, we found that compared to statin users with a vitamin D concentration of 15 ng/mL or higher, those using statins with vitamin D concentration less than 15 ng/mL demonstrated substantially higher odds of musculoskeletal pain (aOR 2.56, 95% CI 1.25, 5.25). Assessment of vitamin D as a continuous variable did not reveal a concentration-related trend between increasing vitamin D concentrations and musculoskeletal pain (p for trend = 0.4). Conclusions: After controlling for multiple confounders, our analyses showed that serum vitamin D concentration less than 15 ng/mL was associated with musculoskeletal pain among statin users. However, among those not using statins, no association between serum vitamin D levels and self-reported musculoskeletal pain was demonstrated. We showed that vitamin D deficiency modifies the relationship between statio use and musculoskeletal pain. Treating vitamin D deficiency has other proven benefits including, bone health and skeletal muscle function. Our data suggests it may be reasonable to identify and treat vitamin D deficiency in patients who report musculoskeletal pain, using statins.
Onyirimba, Esther. "Standardized Clinical Guideline for Assessment, Documentation, and Treatment of Statins." ScholarWorks, 2019. https://scholarworks.waldenu.edu/dissertations/7499.
Full textLowrie, Richard. "A cluster randomised controlled trial of Pharmacist-led Statin Outreach Support in Primary Care." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3352/.
Full textMontazerolghaem, Maryam. "Additives Increasing the Bone-Forming Potential around Calcium Phosphate Cements : Statin, Strontium and Silicon." Doctoral thesis, Uppsala universitet, Tillämpad materialvetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-246289.
Full textLiu, Xiaoling. "Determination of whether the effects of statin drugs are mediated by phosphoinostide 3-kinase." Virtual Press, 2004. http://liblink.bsu.edu/uhtbin/catkey/1306853.
Full textDepartment of Biology
Fulcher, Jordan Ronald. "Studies of Statins, Cholesterol and the Risk of Cardiovascular Disease." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/18205.
Full textAl-Foraih, Meisa. "Dietary, Physical Activity and Other Lifestyle Habits and their Associations with Medication Adherence in a Group of Hypercholesterolemic Patients Prescribed Statin Therapy in Kuwait." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/366088.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Public Health
Griffith Health
Full Text
Proestou, Gregory. "Molecular characterization of clone S44-I, that encodes for a protein antigenically related to statin." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33441.
Full textA WI-38 cDNA library was screened for potential statin clones using the antistatin antibody S44. Clone S44-I was obtained and sequence analysis demonstrated that it shows 99.9% homology to the human C-terminal peroxisomal targeting signal (hPTS1). Northern blot analysis revealed that it is expressed not only in quiescent and senescent, but also in replicating WI-38 as well as in transformed cells. These results suggest that the expression of S44-I is not cell-cycle-arrested-specific.
In vitro translation of S44-I using 35S labeled L-methionine demonstrated that it encodes for a 71 kDa protein which is consistent with the size of the open reading frame (ORF). Moreover, S44-I was transiently transfected and Western blot analysis revealed that S44-I encodes for the expected 71 kDa protein in addition to an 80 kDa polypeptide. Mutation of potential initiation methionines of S44-I for possible alternate initiation of translation mechanism did not eliminate any of the two proteins.
In conclusion, these findings are not consistent with previous studies that have analyzed statin at the protein level. This implies that S44-I does not encode for statin but for the hPTS1 or a related member which may possess a shared antigenic epitope recognizable by the anti-statin antibody.
Wu, Jun. "Statin Medication Adherence and Associated Outcomes in Type 2 Diabetes Medicaid Enrollees with Comorbid Hyperlipidemia." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1276258784.
Full textCirillo, Dominic J. "The effect of statin use on incident immune-mediated and infectious conditions among U.S. veterans." Diss., University of Iowa, 2008. http://ir.uiowa.edu/etd/9.
Full textTissier, Florine. "Effets à long terme de l'atorvastatine à faible dose sur l'athérosclérose : une étude pluridisciplinaire chez un modèle animal, le lapin Watanabe." Thesis, Brest, 2015. http://www.theses.fr/2015BRES0076/document.
Full textCardiovascular diseases are the first worldwide causes of death, associated to the presence and rupture of atherosclerotic plaques. To limit acute events, statins may be prescribed. However, its use leads to deleterious effects risk. To reduce this risk, a dose reduction could be considered. The work of this thesis is to study potential effects of a very low dose of atorvastatin, taken in the long term, in an animal model: the Watanabe rabbit. Measurements are made on control and treated animals from the age of 3 to 12 months. Circulating lipids, biochemical parameters and parameters of adhesion and inflammation were studied. Atherosclerosis evolution was evaluated by optical coherence tomography (OCT). Histological measurements allowed to validate a ranking proposed with OCT observations and to quantify intra-plaque macrophage content. Arterial stiffness was tested in vivo with pulse wave velocity and in vitro with a static tensile test. Vascular function was approached with vasoreactivity in different territories (aorta, carotid, mesenteric). Elastin and collagen contents of the artery wall were determined with two-photon and second harmonic generation microscopy. Finally, mitochondrial respiration and its susceptibility to ROS were evaluated in permeabilized cardiac fibers, any enzymatic antioxidant systems and lipid peroxidation were measured. Results show beneficial effects of this very low dose atorvastatin treatment in cardiovascular function, independently of a lipid-lowering effect.Keywords: atherosclerosis