Relevant bibliographies by topics / Statin

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Statin'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 April 2023

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Journal articles on the topic "Statin"

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Suprapti, Herni. "Pharmacogenomics Statins: Biomarkers for Clinical Prediction." Jurnal Ilmiah Kedokteran Wijaya Kusuma 7, no. 1 (March 30, 2018): 1. http://dx.doi.org/10.30742/jikw.v7i1.61.

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Statins are the most widely prescribed drug for hyperlipidemic therapy and for the prevention of Cardiovascular disease. But although statins are very effective for the prevention of atherosclerosis, there are still patients with CVD. In this case, it is thought to be the influence of genetic factors. There is a static gene link to statin dose required for therapy, but there are still no relevant pharmacogenomic tests for statin therapy guidelines. This article describes basic pharmacogenomic terminology, genes (CETP, HMGCR, SLCO1B1, ABCB1, and CYP3A4 / 5), and progression of statin pharmacogenomic biomarkers for predicted therapeutic outcomes.
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Turkoski, Beatrice B. "One Statin, Two Statins, Three Statins, More." Orthopaedic Nursing 30, no. 1 (2011): 62–65. http://dx.doi.org/10.1097/nor.0b013e318205752a.

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&NA;. "One Statin, Two Statins, Three Statins, More." Orthopaedic Nursing 30, no. 1 (2011): 66–67. http://dx.doi.org/10.1097/nor.0b013e3182099340.

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Ma, Wei-li, Yu Yun Shao, Chih-Hung Hsu, Kun-Huei Yeh, Ho-Min Chen, Yi-Chun Yeh, Chiu-Lin Lai, Zhong-Zhe Lin, Ann-Lii Cheng, and Mei-Shu Lai. "Regular statin users and colorectal cancer (CRC) prognosis." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 3554. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3554.

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3554 Background: Statins are frequently used for the control of hyperlipidemia. Statins have multiple anti-cancer properties and may be associated with lower CRC risks among their users. This study tries to go a step further and explores whether statin use affects the prognosis of curatively resected CRC. Methods: We established a population cohort with patients (age ≥ 40 y) who were diagnosed as having stage I or II CRC from 2004 to 2008 and received curative surgery from the database of Taiwan Cancer Registry. Data of medication prescription and co-morbidities were retrieved from the database of National Health Insurance, Taiwan. Regular statin use was defined as taking statins for > 180 days within the observation period from one year before the cancer diagnosis to one year afterward. The database of National Death Registry was used for survival outcomes. Another similar cohort consisting of patients with hepatocellular carcinoma (HCC) was used for comparison. Results: In total, 10762 patients with CRC were enrolled; 891 (8%) patients were regular stain users, 812 (8%) patients took statins but were not regular users, and 9059 (84%) patients never used statins. Regular statin users, compared to never users, were more likely to be female (p < 0.001), older (p < 0.001), have stage I disease (p < 0.001) and co-morbidities such as diabetes, coronary artery disease, and renal disease. Adjuvant therapy was less frequently administered in regular statin users. In univariate analysis, cancer-specific survival (CSS) of regular stating users was significantly longer than that of never users (5-y CSS, 87% vs. 84%, p = 0.022), but overall survival (OS) was not significantly different (5-y OS, 80% vs. 77%, p = 0.156). In multivariate analysis adjusting for age, gender, stage, adjuvant therapy, co-morbidities, and the use of aspirin, regular stating use was an independent predictor both for better CSS (hazard ratio [HR] 0.72, p < 0.001) and for better OS (HR 0.71, p< 0.001). In contrast, no associations were found between statin use and CSS or OS in the HCC comparison cohort. Conclusions: Regular statin use was associated with better prognosis in CRC patients who received curative therapy. (This study was supported by grants DOH-101-TD-B-111-001 and DOH-102-TD-B-111-001).
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Son, Kyung-Bok, and SeungJin Bae. "Patterns of statin utilisation for new users and market dynamics in South Korea: a 13-year retrospective cohort study." BMJ Open 9, no. 3 (March 2019): e026603. http://dx.doi.org/10.1136/bmjopen-2018-026603.

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ObjectiveThis study analysed utilisation of statins for new statin users and assessed market dynamics of statins in South Korea.DesignThis study is a retrospective cohort study.SettingThe yearly claims data for statins were retrieved from the National Health Insurance Service-National Sample Cohort.Main outcome measureWe are interested in new statin users during 2003–2015 in Korea. Information on prescribed statins, including intensity of statins and entry of new and follow-on statins in the market, and healthcare institutions that prescribed the statins were also collected. In time series analysis, we estimated the effect of introduction of generics in the market, specifically for newly prescribed statin users.ResultsThis 13-year longitudinal study of a sample cohort provided by the National Health Insurance Service found that the incidence of new statin user increase from 838.1/100 000 persons in 2003 to 1626.9/100 000 persons in 2015. Most new users were initiated on a monotherapy that was prescribed at primary healthcare institutions. However, the statin market for new users were quite dynamic in Korea. First, the most commonly prescribed statin changed several times during the study period. Second, the use of moderate-intensity statins increased from 57% in 2003 to 92% in 2015. In line with this result, we could not observe substantial differences in prescription of statins in groups having selected diseases history. Lastly, we found market invasion or switch of statins among new statin users, specifically at primary healthcare institutions.ConclusionSimilar to other countries, the incidence of new statin users has been increased in Korea. However, the statin market in Korea is quite dynamic compared with other countries. Interestingly, discounted price of originals after the introduction of generics immediately expand markets or substitute the market particularly in primary healthcare institutions in Korea.
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Abdullah, Kazeen, and Anand Rohatgi. "Statins: Practical Considerations – A Review." European Cardiology Review 9, no. 2 (2014): 71. http://dx.doi.org/10.15420/ecr.2014.9.2.71.

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Statins are currently the most efficacious and widely prescribed lipid-lowering medications. The 2013 ACC/AHA cholesterol guidelines provide a dramatic shift in treatment approach with a focus on fixed-dose statins matched to individual risk scores. Statin intolerance is not uncommon and can be challenging to diagnose and manage; however, several therapeutic strategies have been successful in achieving statin tolerance. Statin use is also associated with liver enzyme elevations and increased risk of incident diabetes, but studies show these individuals benefit from statins. Several guidelines exist and statin use is expected to increase with the new cholesterol guidelines bringing along new challenges for prescribers. This review article will provide practical considerations for statin use and management of statin intolerance.
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Bubnova, Marina G. "Adverse effects of statin therapy: real evidence." CardioSomatics 10, no. 1 (March 15, 2019): 51–61. http://dx.doi.org/10.26442/22217185.2019.1.190264.

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Aim. To provide a current view on the tolerability and safety of statin therapy. Materials and methods. The data of 73 scientific sources from Russian and foreign literature published within 1996-2018 are considered. Results. It is generally accepted that statins are first-line therapeutic agents for hypercholesterolemia and combined hyperlipidemia. Today there in growing evidence that lowering of low-density lipoprotein cholesterol levels prevents atherosclerotic diseases and reduces a risk of cardiovascular and overall mortality. Main issues of current statin therapy include a use of inadequate dosage for atherosclerotic diseases prevention, low treatment compliance and drug intolerance. In recent years the issue of statin intolerance has become of great importance. Criteria were proposed for determining an inability to tolerate statins, some experts suggest replacing definition of “statin intolerance” with the term “statin-associated side-effects”. Most discussed adverse effects due to statins include muscle-related symptoms (myalgia/myopathy), hepatotoxicity (hepatic hyperenzymemia) new-onset diabetes, dementia and cognitive impairment. Mechanisms of development of these adverse effects are still unclear. Certain factors and conditions capable of triggering some adverse effects as well as absolute contraindications to statin therapy were established. Some factors and conditions capable of triggering some adverse effects as well as absolute contraindications to statin therapy were identified. Occurrence of statin-associated side-effects depends on statin dose, a patient's age, gender, comorbidity and concomitant therapy. Many adverse effects of statins are drug class effect. At the same time each of statins has specific features of its structure, metabolism, drug interactions and pharmacokinetics. Pitavastatin belongs to the last generation of statins and it has distinct pharmacological features and neutral diabetogenic effects, etc. Risk of adverse effects due to statins is often exaggerated while benefit from the use of statins for preventing atherosclerotic diseases outweighs potential risks. Real occurrence of some adverse effects due to statin therapy requires additional evidence. Conclusion. Overall, statins have a good tolerability profile and are approved for use in the vast majority of patients who required lipid-lowering therapy.
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Khanna, Roopali, and Dandu Himanshu. "Statin Intolerance: Diagnosis and Management." Indian Journal of Cardiovascular Disease in Women WINCARS 02, no. 03 (September 2017): 014–20. http://dx.doi.org/10.1055/s-0037-1607193.

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AbstractStatins are the main cornerstone in the treatment of coronary artery disease. Statins not only reduce the cardiovascular events but also significantly reduce the all-cause mortality. Due to adverse effects of statins, 20 to 30% of patients discontinue statins without consulting the physician. Most common adverse effects reported are muscle symptoms. Studies have shown that the majority of these patients can tolerate statin upon rechallenge. Alternative statin dosing, alternate-day statin, or twice-weekly statin dosing are different strategies to be given before changing to nonstatin lipid-lowering therapy. The newer nonstatin lipid-lowering drugs (ezetimibe, PCSK9 inhibitors) can be added if the low-density lipoprotein (LDL) target level can be achieved despite the maximally tolerated statin dose. This article reviews the etiology, clinical symptoms, and management of statin intolerance.
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DeWitt, Cassandra M., Robert B. Ponce, Hayley Bry, Soma Wali, Erica Sedlander, and Joseph A. Ladapo. "Patient-Reported Reasons for Not Using Primary Prevention Statin Therapy." Journal of Clinical Medicine 9, no. 10 (October 18, 2020): 3337. http://dx.doi.org/10.3390/jcm9103337.

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Almost half of patients who meet American College of Cardiology/American Heart Association (ACC/AHA) criteria for statin therapy are untreated. We aimed to evaluate patient-reported reasons for not using guideline-recommended statin therapy in a public healthcare system. Achieving this goal is key to addressing gaps in care and reducing preventable cardiovascular morbidity. We surveyed patients who met 2013 ACC/AHA guidelines for statin therapy but were not using statins. The survey probed domains of patient knowledge regarding cardiovascular health and benefits of statins, barriers to use, physician trust, and interest in cardiovascular care. Among 71 patients eligible for guideline-recommended statin therapy but not currently taking statins, 49 (69%) had a high school education or lower, 41 (58%) reported that they were unaware they should be prescribed a statin and 49 (69%) were unaware of the benefits of statins. Almost all patients, 70 (99%), reported caring about their cardiovascular health, 61 (86%) reported that they had a high level of trust in their physician, and 51 (72%) reported a willingness to follow their physician’s advice. Despite interest in cardiovascular health, awareness of benefits of statin therapy was low and knowledge of recommended statin therapy was low. Increasing patients’ awareness of their eligibility through systematic testing and linkage to statin therapy, along with education, may increase statin use among patients recommended for therapy.
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McBride, Cameron L., Julia M. Akeroyd, David J. Ramsey, Vijay Nambi, Khurram Nasir, Erin D. Michos, Ruth L. Bush, et al. "Statin prescription rates and their facility-level variation in patients with peripheral artery disease and ischemic cerebrovascular disease: Insights from the Department of Veterans Affairs." Vascular Medicine 23, no. 3 (March 30, 2018): 232–40. http://dx.doi.org/10.1177/1358863x18758914.

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The 2013 American College of Cardiology/American Heart Association cholesterol guideline recommends moderate to high-intensity statin therapy in patients with peripheral artery disease (PAD) and ischemic cerebrovascular disease (ICVD). We examined frequency and facility-level variation in any statin prescription and in guideline-concordant statin prescriptions in patients with PAD and ICVD receiving primary care in 130 facilities across the Veterans Affairs (VA) health care system between October 2013 and September 2014. Guideline-concordant statin intensity was defined as the prescription of high-intensity statins in patients with PAD or ICVD ≤75 years and at least moderate-intensity statins in those >75 years. We calculated median rate ratios (MRR) after adjusting for patient demographic factors to assess the magnitude of facility-level variation in statin prescribing patterns independent of patient characteristics. Among 194,151 PAD patients, 153,438 patients (79.0%) were prescribed any statin and 79,435 (40.9%) were prescribed a guideline-concordant intensity of statin. PAD patients without ischemic heart disease were prescribed any statin and a guideline-concordant intensity of statin therapy less frequently (69.1% and 28.9%, respectively). Among 339,771 ICVD patients, 265,491 (78.1%) were prescribed any statin and 136,430 (40.2%) were prescribed a guideline-concordant intensity of statin. ICVD patients without ischemic heart disease were prescribed any statin and a guideline-concordant intensity of statin less frequently (70.9% and 30.5%, respectively). MRRs for both PAD and ICVD patients demonstrated a 20% and 28% variation among two facilities in treating two identical patients with statin therapy and guideline-concordant intensity of statin therapy, respectively. The prescription of statins, especially guideline-recommended intensity of statin therapy, is suboptimal in PAD and ICVD patients, with significant facility-level variation not explained by patient-level factors.
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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.

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Statins are the mainstay of cholesterol-lowering therapy and are taken by millions of people worldwide. These drugs are generally well-tolerated but can cause myopathy ranging from mild muscle pain to fatal rhabdomyolysis. The mechanism of statin-induced myopathy (SIM) is not fully understood and there is currently no convenient and reliable marker of SIM, but mitochondrial dysfunction has been implicated. We sought to investigate the effect of statins on mitochondrial DNA (mtDNA) levels in order to gain information on the mechanism of SIM and to explore the possibility of utilizing changing mtDNA levels as a marker of SIM. Several approaches were used. First, mtDNA levels were quantified in skeletal muscle biopsies collected from a previously published 8-week clinical trial of high-dose simvastatin or atorvastatin versus placebo. Forty-eight hypercholesterolemic subjects were randomly assigned to receive placebo (N=16), high dose atorvastatin 40mg/day (N=16), or high dose simvastatin 80mg/day (N=16) for 8 weeks. Muscle mtDNA content was assessed by real-time PCR atbaseline and after 8-weeks on statin treatment and found to be significantly reduced in the groupreceiving simvastatin (P=0.005) but not the other two. In addition, a significant positive correlation was observed between mtDNA and muscle ubiquinone in all groups (R=0.63, P<0.01), with the strongest association found in the simvastatin-treated subjects (R=0.75, P=0.002). Next, in an attempt to determine whether statin-induced muscle pain may be associated with muscle mtDNA depletion, archived muscle biopsies collected from statin users with muscle complaints were sought through a review of a muscle biopsy database and possible study samples were identified; however, this was put on hold as too much information was missing from the pathology reports. Third, a series of cell culture experiments were carried out in which human skeletal muscle myotubes were exposed to various concentrations of simvastatin or atorvastatin, in order to determine an appropriate dose range for subsequent mitochondrial toxicity experiments. Lastly, mtDNA content and expression was quantified in skeletal muscle biopsies collected from 10 patients with statin-induced rhabdomyolysis (SIR) and compared to 8 healthy controls to investigate whether muscle mtDNA is altered in rhabdomyolysis. No differences in mtDNA content or expression were observed between the two study groups, but this may have been be due to the SIR subjects' marked heterogeneity. Statin therapy can be associated with considerable alterations in mtDNA content, which may play a role in the aetiology of SIM. MtDNA levels alterations with statin exposure should be investigated further to explore the involvement of mitochondrial alterations in the mechanism of SIM, and determine whether these may represent a useful clinical tool for assessing statin-induced muscle toxicity.
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Siddiqui, Moneeza Kalhan. "Genetic factors in statin intolerance." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/5852fdf4-5737-4c23-a391-f0bc4e627ebb.

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Background: There are approximately 12 million statin users in the United Kingdom. Reports of statin intolerance occurs between 7 and 29% of users, manifesting as muscle ache, fatigue or more seriously, muscle breakdown leading to myopathy. Creatine phosphokinase (CK) levels are used as a biomarker of statin-induced muscle damage. Non-adherence or discontinuation of therapy is a common result of intolerance and can result in negative cardiovascular disease-related outcomes. Aim: This thesis attempts to identify trends in record-linked medical data in a Scottish Caucasian cohort (GoDARTS) that best represent statin intolerance in order to study associated genetic factors. Methods: Prescribing trends such as switching or discontinuation of statin therapy were examined, and thresholds created to select true cases of intolerance. Information on CK levels was gathered from medical records and appropriate test results were utilized. Genotypic data was gathered for the variants and genetic regions of interest using a variety of methods including chip-based genotyping followed by imputation, TAQMAN genotyping, and exome sequencing. Subsequently hypothesis-based association analyses were conducted, including linear and logistic regressions, followed by meta-analyses, regional GWAS followed by a regional meta –analysis. Results: The phenotypes of statin intolerance were validated both internally and externally. Previously reported missense variants in LILRB5 (Asp247Gly) and CKM (Glu83Gly) were replicated and shown to be associated with CK levels irrespective of statin usage in the GoDARTS cohort and the clinical trial setting (JUPITER). Further, the CKM variant was also associated with inducibility of CK at times of tissue injury. The Asp247 genotype in LILRB5 was associated with increased risk of statin intolerance, and was replicated in associations with non-compliance to statin therapy and the development of myalgia in the JUPITER trial. The association with myalgia showed a stratified effect based on therapy (statin or placebo), with those on placebo showing the genotype effect. Further, the variant was also associated with increased risk of statin-induced myositis, cases of which had been clinically adjudicated and exome sequenced for the PREDICTION-ADR consortium. Further exploration of the LILR gene region showed an association with variants in LILRB2 (His20Arg and Val235Met) which were in strong LD with each other but were not in linkage with the variant in LILRB5. Stratified analysis revealed that the risk for carriers of the LILRB2 variants was increased depending on the genotype carried at the LILRB5 variant. Conclusions: This study characterises novel genetic factors associated with statin intolerance impacting adherence. The findings point to the immunomodulatory effects of statins. The results suggest that true statin-induced myalgia and non-specific myalgia are distinct, with a possible role for the immune system in their development. The findings encourage further investigation into the immune-physiology of statin-induced muscle damage and identifies genetically susceptible groups who are more likely to be statin intolerant.
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Wong, 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.

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Mack, Deborah Sara. "Statin Pharmacotherapy in U.S. Nursing Homes." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1104.

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Background: Statins have questionable benefits among older adults with life-limiting illness. Statin use is widespread among U.S. older adults, but little is known about use in nursing homes. This dissertation was designed to identify the prevalence and predictors of statin pharmacotherapy use and discontinuation in U.S. nursing homes. Methods: Data sources (2011-2016) included: Minimum Data Set 3.0, Medicare administrative claims data, Provider of Service files, and Dartmouth Atlas files. Analyses included: descriptive statistics, multilevel modeling, and proportional change in cluster variations with adjustments to reduce confounding and model misspecification. Results: Approximately 36% of older adults admitted to U.S. nursing homes between 2015 – 2016 were actively using statins at the time of admission. Among long-stay residents with life-limiting illness, 34% were on statins at one time (2016; aged 65-75 years: 44%, >75 years: 31%). Statin use varied significantly by hospital referral regions, with most variation in the >75 age group. Limiting the sample to statin users, 20% discontinued statins within 30 days of nursing home admission. While discontinuation was positively associated with severity of life-limiting condition, the majority of residents remained on statins 30 days post-admission, including those with a < 6-month prognosis. Conclusion: Statin use is pervasive across US nursing homes and persists with life-limiting illness. Geographic variation appeared to coincide with clinical uncertainty, especially among adults >75 with few national guidelines. More needs to be done to prioritize statin deprescribing in nursing homes with research that identifies ways to facilitate improved patient-provider awareness and engagement in the discontinuation process.
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Wong, 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.

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Stringer, Henry. "Mitochondrial DNA alterations and statin-induced myopathy." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/9949.

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Background/Objectives: Statins are widely used to treat hyperlipidemia and lower cardiovascular disease risk. While statins are generally well tolerated, ~10-15% of patients experience statin-induced myopathy (SIM), a potentially fatal complication. Statin treatment has been associated with mitochondrial dysfunction. High-dose simvastatin treatment has been associated with skeletal muscle mitochondrial DNA (mtDNA) depletion. The contribution of mitochondrial dysfunction to the development and exacerbation of SIM may be important. The goal of this project was to examine the effects of statins on mtDNA to provide further insight into the etiology and severity of mitochondrial myotoxicity in SIM. Methods/Results: Two studies were performed. PCR quantification of mtDNA and nuclear DNA was used to measure mtDNA content. Long-template PCR was used to amplify the mitochondrial genome and score mtDNA deletion burden. In an in vitro study, rhabdomyosarcoma cells were exposed to simvastatin and atorvastatin for over 70 days. Both mtDNA content and deletion burden were measured longitudinally and remained unchanged amongst statin treated cells. In an in vivo study, skeletal muscle biopsies from patients diagnosed with SIM (n=24) and comparators showing no pathologic findings (n=23) were retrospectively reviewed from stored clinical samples. The pathologic features and degree of pathology within each biopsy were scored. MtDNA content and deletion score was compared between groups. Two genotypes that are associated with changes in statin response and SIM risk, apolipoprotein E and SLCO1B1, were examined. No difference in genotype frequency between groups was detected. Controlling for age, gender, biopsy year and apolipoprotein E genotype, SIM subject mtDNA/nDNA (mean±SD, 2036±1146) was significantly lower than the comparators (3220±1594) (p=0.042). No difference was observed in mtDNA deletion score (0-200) between SIM subjects (21.2±19.2) and comparators (19.4±30.0). There was an inverse correlation between mtDNA content and degree of pathology (p=006 r=-0.399). Conclusions: We found decreased in vivo skeletal muscle mtDNA content in association with SIM. How this relates to the pathogenesis of SIM remains unclear. As the mtDNA deletion score was not associated with SIM, quantitative rather than qualitative mtDNA alterations are suggested. MtDNA content should be further investigated as a potential marker of statin drug myotoxicity.
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Timoney, 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.

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Link, 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.

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Lowering LDL-cholesterol with statin therapy produces substantial reductions in cardiovascular events, and larger cholesterol reductions may produce larger benefits. Rarely, myopathy occurs with statins, especially at higher doses and in combination with certain medications. Similarly strong associations might exist between myopathy with high-dose statin regimens and genetic variants, especially those affecting blood statin levels. This study aimed to find genetic variants associated with statin-induced myopathy. A feasibility study was completed to assess whether plausible effect sizes of 5 to10-fold higher risks per genetic variants could be detected among 50-100 cases with statin-induced myopathy and to consider the best study design. A genome-wide association study was then carried out using approximately 300,000 genetic markers (and additional fine-mapping) in 85 people with definite or incipient myopathy and 90 controls, who were all taking 80mg simvastatin daily in a 12,000 participant trial of 80mg vs 20mg simvastatin daily. The cases were also compared to 2,300 additional controls who had not been exposed to intensive-dose statin therapy. Replication of the myopathy result and lipid-lowering associations were tested in a 20,000 participant trial of 40mg simvastatin daily versus placebo. The genome-wide scan yielded a single strong association (p = 4x10-9) of myopathy with the rs4363657 single nucleotide polymorphism (SNP) located within the SLCO1B1 gene on chromosome 12. This non-coding SNP was in nearly complete linkage disequilibrium (r2=0.97) with the non-synonymous rs4149056 SNP. The population prevalence of the rs4149056 C allele was 15%, and the odds ratio for myopathy was 4.5 (95% confidence interval 2.6 to 7.7) for each copy of the C allele and 16.9 (4.7 to 61.1) for CC vs TT homozygotes. Over 60% of these myopathy cases could be attributed to the C variant. The SLCO1B1 gene encodes the organic anion transport polypeptide OATP1B1, which has been shown to regulate hepatic uptake of statins. In literature reports, rs4149056 reduced statin transport and was associated with 37% (31% to 44%) higher systemic statin acid levels per C allele. The association of rs4149056 with myopathy was replicated in the trial of 40mg simvastatin daily, which also showed that it was associated with the cholesterol-lowering effects of simvastatin. No SNPs in any other region were clearly associated with myopathy (although comparison of the myopathy cases with the 2,300 controls identified a region of chromosome 1p12 that warrants further study). This study identified common variants in SLCO1B1 that influence the risks of statin-induced myopathy substantially. Genotyping these variants may be useful for tailoring both the statin dose and safety monitoring. More generally, such studies of the genetic determinants of serious adverse reactions with other drug classes may help to improve the balance between treatment efficacy and safety.
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Boyle, Ashley Kathryn. "Effect of statin treatment on preterm labour." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29558.

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Preterm labour (PTL) is defined as labour before 37 completed weeks of gestation. Despite advances in medical research, PTL remains a major clinical problem. Preterm birth (PTB) rates range from approximately 5-18% worldwide. Importantly, PTB is the leading cause of childhood morbidity and mortality. PTL is difficult to predict and the aetiology is poorly understood but infection and inflammation are believed to be major factors. It has been suggested that the presence of intrauterine infection or inflammation may initiate the pathological, preterm activation of the inflammatory cascade associated with term labour. Therefore, PTL therapeutics should aim to inhibit these inflammatory pathways. Statins, 5-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, are potent inhibitors of cholesterol biosynthesis, which act on the mevalonate pathway. In addition to their lipid-lowering effects, statins also have anti-inflammatory and anti-contraction properties. The hypothesis of this thesis was that statins will prevent PTB by reducing inflammation. The aims of this thesis were firstly to investigate the effect of the statins, simvastatin and pravastatin, on inflammation and contractility in a pregnant human myometrial cell line. Secondly, to determine whether simvastatin and/or pravastatin can prevent PTB or improve neonatal outcome in a lipopolysaccharide (LPS)-induced mouse model of PTB. Myometrial cells were either co-treated with LPS and simvastatin/pravastatin, pretreated with simvastatin/pravastatin or treated with simvastatin/pravastatin post-LPS stimulation. The effect of statin treatment on the mRNA expression and the release of inflammatory mediators was then investigated. Simvastatin treatment reduced LPS-induced inflammation by both lowering the expression of pro-inflammatory mediators and increasing the expression of anti-inflammatory mediators. Pravastatin treatment did not alter the expression of inflammatory mediators following LPS stimulation. The effect of simvastatin on the contraction of myometrial cells was investigated by embedding the cells in rat tail collagen to form gels. As these are smooth muscle cells, basal contraction was observed causing the gel size to reduce. When LPS was introduced, this caused the gels to contract further than the vehicle treated gels. Simvastatin attenuated the contraction of the myometrial cells, both alone and in the presence of LPS. These effects were reversed by the addition of mevalonate pathway metabolites, mevalonate and geranylgeranyl pyrophosphate (GG-PP) but not by farnesyl pyrophosphate (F-PP). Simvastatin also lowered levels of phosphorylated myosin light chain (pMLC) in the myometrial cells, which is essential for smooth muscle contraction. Again, this effect was abolished by mevalonate and GG-PP but not F-PP. It is hypothesised that simvastatin attenuated myometrial cell contraction by inhibiting Rho isoprenylation by GG-PP, preventing Rho-associated kinase (ROCK) activation, which then prevented the phosphorylation of MLC. A mouse model of intrauterine LPS-induced PTB was utilised to investigate the effect of statin treatment on PTB and fetal survival. Mice received an intraperitoneal injection of pravastatin (10μg) or simvastatin (20μg or 40μg) on gestational day (D)16. This was followed by ultrasound-guided intrauterine injection of LPS (1μg) on D17 and another pravastatin/simvastatin treatment two hours later. When mice were treated with LPS, 77.8% of mice delivered preterm. When mice received LPS and 20μg simvastatin, 50% delivered preterm. However, when mice were treated with LPS and 40μg simvastatin, 40% delivered preterm, more pups were born alive and uterine pro-inflammatory mRNA expression was downregulated. Conversely, pravastatin did not prevent PTB or improve the percentage of live born pups. In summary, simvastatin treatment exerted anti-inflammatory and anti-contraction effects on human myometrial cells in vitro. The anti-contractile properties were likely due to the inhibition of the Rho/ROCK pathway. Furthermore, in our LPS-induced mouse model of PTB, fewer mice delivered preterm with simvastatin treatment, simvastatin attenuated LPS-induced pup mortality and reduced uterine inflammatory gene expression. These results suggest that statin therapy may be a novel treatment for PTL.
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Ostrowski, 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.

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Books on the topic "Statin"

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Statin prescribing guide. Oxford: Oxford University, 2010.

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Thompson, Paul D., and Beth A. Taylor, eds. Statin-Associated Muscle Symptoms. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33304-1.

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A, Wong B., ed. Focus on statin research. New York: Nova Science Publishers, 2005.

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Misbahuddin. Statin Pharmacogenetics in Metabolic Syndrome- The SREBP-SCAP Pathway. Germany: LAP LAMBERT Academic Publishing, 2012.

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M, Pickin D., and Trent Institute for Health Services Research. Working Group on Acute Purchasing., eds. Statin therapy / HMG Co-A reductase inhibitor treatment in the prevention of coronary heart disease. Sheffield: Trent Institute for Health Services Research, 1996.

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Bowden, Jonny. The Great Cholesterol Myth: Why lowering your cholesterol won't prevent heart disease-- and the statin-free plan that will. Beverly, MA: Fair Winds Press, 2012.

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Reinhold, Ulrich. Diastereo- und enantioselektive Synthese von 1,2-Aminoalkoholen und [alpha]-Hydroxyaldehyden [Alpha-Hydroxyaldehyden] aus chiralen Glykolaldehyd-Hydrazonen: Asymmetrische Synthese von (R, R)-Statin. [S.l: s.n.], 1995.

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What you must know about statin drugs & their natural alternatives: A consumer's guide to safely using lipitor, zocor, mevacor, crestor, pravachol, or natural alternatives. Garden City Park, N. Y: Square One Publishers, 2005.

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H, Acquaviva Thomas, and Lewis Research Center, eds. Static stability of the space station solar array FASTMast structure. Cleveland, Ohio: NASA Lewis Research Center, 1995.

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Stalin. New York, N.Y., U.S.A: Puffin Books, 1993.

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Book chapters on the topic "Statin"

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Schaefer, Jochen, and Sandra Jackson. "Statin Myopathy." In Acquired Neuromuscular Disorders, 137–47. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06731-0_8.

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Schaefer, Jochen, and Sandra Jackson. "Statin Myopathy." In Acquired Neuromuscular Disorders, 113–22. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29514-5_8.

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Mitchell, Brian. "The Statin Trilogy (I): ‘Statin’ from the Beginning." In A Case Approach to Perioperative Drug-Drug Interactions, 619–22. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-7495-1_137.

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Benatar, Michael. "Statin-Induced Myopathy." In Neuromuscular Disease, 389–95. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-106-2_21.

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Seip, Richard L., Jorge Duconge, and Gualberto Ruaño. "Genotype-Guided Statin Therapy." In Pharmacogenomic Testing in Current Clinical Practice, 155–74. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-283-4_10.

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Bartlomiejczyk, Marcin A., Peter E. Penson, and Maciej Banach. "Management of Statin Intolerance." In Contemporary Cardiology, 207–18. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56514-5_12.

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Mitchell, Brian. "The Statin Trilogy (II): Tripped and Fell at the Train ‘Statin’." In A Case Approach to Perioperative Drug-Drug Interactions, 623–26. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-7495-1_138.

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Goldberg, Stanley J. "Non-Statin Treatment of Dyslipidemia." In Lipid Management, 201–31. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11161-2_12.

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Superko, H. Robert, Tom White, James Forrester, and Spencer King. "The Statin Response Gene: KIF6." In Pharmacogenomic Testing in Current Clinical Practice, 175–98. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-283-4_11.

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Newman, Connie B., and Jonathan A. Tobert. "Statin-Related Myopathy and Rhabdomyolysis." In Endocrine and Metabolic Medical Emergencies, 760–74. Oxford, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119374800.ch45.

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Conference papers on the topic "Statin"

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Carvalho, Ana Cláudia Pires, Fernanda Rezende Dias, Luisa Crevelin Costa, and Natália de Castro Fim Nakao. "Myopathy following statin use." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.512.

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Introduction: Myopathies can be caused by various drugs, including statins and corticosteroids, and can be toxic or inflammatory, one example being necrotizing myositis triggered by statins. Objectives: Describe the case of a patient with weakness after statin use. Design and setting: Case report Methods: Analysis of medical record, photographic record of the diagnostic methods and literature review. Case description: 69-year-old female, obese, hypertensive, diabetic, dyslipidemic and hypothyroid, taking atorvastatin since 2017, referred by endocrinology for generalized myalgia in 2019, with increased creatine phosphokinase (CPK). Discontinued statin use since then, maintaining symptoms. Neurological examination showed tetraparesis, with proximal predominance. Electroneuromyography (ENMG) showed signs of myopathy. Corticotherapy with deflazacort was initiated, with improvement of symptoms and reduction of CPK levels. Investigation for paraneoplastic syndrome was performed, with negative results. He started using pioglitazone, prescribed by endocrinology, with reduced corticotherapy, for better glycemic control, presenting worsening weakness, frequent falls, and dyspnea on effort. The patient repeated ENMG in one month, without changes. Performed an anti-HMG-CoA reductase autoantibody test, with a positive result, concluding the diagnosis of immune-mediated necrotizing myositis triggered by statins, with a probable toxic myopathy after use of pioglitazone. Azathioprine was introduced, with gradual weaning from corticosteroids, and physical therapy was started. Conclusion: Several medications can cause myopathy, directly (toxic) or indirectly (immune-mediated), and this patient used 3 potentially myopathy-causing drugs (atorvastatin, deflazacort, and pioglitazone). The nonimprovement upon medication withdrawal suggested an immune-mediated inflammatory cause, confirmed in this case by the determination of a specific autoantibody for statin-induced necrotizing myositis.
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Lalic, Kristina, Jasna Tekavec Trkanjec, Marija Šimic, and Neven Tudoric. "Statin-induced lung diseases." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa834.

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Dick, Melissa, and Richard L. Leask. "Effect of Statins and Wall Shear Stress on Endothelial Cells: Morphology and F-Actin Cytoskeleton Arrangement." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80585.

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Wall shear stress and statin drugs have both been shown to influence endothelial cell function. We investigated the effect of statins on the morphology and F-actin cytoskeleton arrangement of endothelial cells with and without wall shear stress. Under static conditions, statins caused cells to become rounded and disorganized the F-actin cytoskeleton. Wall shear stress abrogated the morphological effects, but did not reverse the cytoskeleton disorganization.
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Daban, Alaa Hasan. "The prevalence of statin prescription for primary prevention of Arteriosclerotic Cardiovascular Diseases among patients with Type 2 Diabetes in Qatar." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0098.

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Background: Qatar has one of the highest prevalence rates for diabetes in the world. Arteriosclerotic cardiovascular diseases (ASCVDs) are responsible for nearly 50% of deaths among patients with diabetes in Qatar. Treating with statins is a simple and effective approach for preventing ASCVD among patients with diabetes. Local and international guidelines recommend the use of statins for primary prevention of ASCVD in patients with diabetes, especially for those 40-75 years of age. Yet statins are still under-prescribed to diabetic individuals for primary prevention of ASCVD worldwide, especially in primary care settings which is where most of the medical management of diabetes occurs. Little is known about the prevalence of statin prescription for primary prevention of ASCVD among diabetics in primary care settings in Qatar. Objectives: To measure the proportion of T2dm patients receiving statins for primary prevention of ASCVD in primary care settings and to investigate patients’ characteristics associated with statin prescription. Results: Of 23,934 patients with complete data, 57% were males and 31.9% were Qatari nationals. Average age for participants was 54.8 ± 8.25 years. 66 % of the patients received statins at least once during the year 2019. The statin prescription rate for Non-Qatari males was 70.1% and was significantly higher than non-Qatari females, Qatari females, or Qatari males (62.2%, 62.9% and 63.9% respectively P value <0.000) In a multivariable model analysis and after controlling for other covariates in the model, statin prescription was positively associated with being male (adjusted odds ratio (aOR): 1.2, [95% CI: 1.12-1.28]), history of smoking, i.e. former smoker (aOR 1.16 [95% CI: 1.03-1.29]), current smoker (aOR 1.11 [95% CI: 1.01-1.22 ]), associated diagnosis of hypertension (aOR 1.51 [95% CI: 1.41-1.61]), being prescribed other non-statin lipids lowering medications (aOR 1.44 [95% CI: 1.27-1.63]), increased age (aOR 1.03/year [95% CI: 1.026-1.034]), increasing daily pill burden (aOR 1.23/pill [95% CI: 1.21-1.25]), increasing number of daily medication injections (aOR 1.29/injection [95% CI: 1.23-1.35]), and frequent visits to GP clinic (aOR 1.22/visit [95% CI: 1.19-1.24]). Statin prescription was negatively associated with having a history of diabetic neuropathy (aOR 0.87 [95% CI: 0.75-1.0]), increasing BMI (aOR 0.996/unit [95% CI: 0.9892-1.00]), being Qatari (aOR 0.87 [95% CI: 0.81-0.93]) or being prescribed an anti-platelet (aOR 0.96/unit [95% CI: 0.89-1.03]). Significant negative effect modification between hypertension and either male gender or Qatari nationality was found, further lowering the odds for Qatari males. Conclusion: Prevalence of statin prescription for primary prevention of ASCVD among patients with T2dm was suboptimal in primary care settings in Qatar and need to be improved. Factors associated with a lower prevalence of statin prescription namely female gender and Qatari nationality needs to be addressed. Further studies are needed to explore causes of the low prescription rates of statins in Qatar.
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Zeki, A. A., K. Chmiel, and O. Fiehn. "Statin Drug Lipophilicity Affects Airway Epithelial Distribution: Not All Statins Are Created Equal." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2170.

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Saad, Nathalie, Pierre Ernst, Philippe Camus, and Sammy Suissa. "Statin-Induced Interstitial Lung Disease (SI-ILD)." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3038.

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Syifa, Nailis, Cici Dwi, and Didik Hasmono. "Drug Utilization Study of Statin in Hemorrhagic Stroke." In Health Science International Conference (HSIC 2017). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/hsic-17.2017.45.

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Mallah, H., A. Wichmann, J. Makram, I. Prufer, J. Sekhon, and A. Yepes-Hurtado. "A Rare Case of Statin-Induced Necrotizing Myositis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1364.

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Rossi, Joanna, Léonie Rouleau, Jean-Claude Tardif, and Richard L. Leask. "Fluid Shear Stress Reduces Simvastatin Induced Adhesion Molecule Expression in Cytokine Activated Endothelial Cells." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206539.

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Although originally designed as inhibitors of cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are now known to also have non-lipid lowering benefits [1]. Statins have been reported to modulate gene expression in endothelial cells, however, the effect of statins on adhesion molecule expression is contradictory. Some studies report a decrease in adhesion molecule mRNA and/or protein after statin treatment [2], while others have shown that statins potentiate the effect of tumor necrosis factor alpha (TNFα) [3]. To the best of our knowledge, the effects of statins on gene expression in cultured endothelial cells has been done in static conditions only and no study has examined the effect of blood flow. This is particularly important since fluid shear stress is a strong regulator of endothelial cell function and phenotype [4]. The purpose of this study was to clarify the effects of statins on vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) expression in endothelial cells by evaluating their biological response under fluid flow.
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Cerdá Iñesta, J., F. Wirth, G. Zahra, RG Xuereb, C. Barbara, and A. Serracino-Inglott. "5PSQ-021 Pharmacogenetic testing for personalisation of statin therapy." In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.454.

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Reports on the topic "Statin"

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LI, Peng, and Junjun Liu. Effect of statin therapy on moderate-to-severe depression: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0016.

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Review question / Objective: We aim to assess the antidepressant effects of statin therapy among patients complicated with moderate to severe depression. Condition being studied: Depression is one of the major causes of disability worldwide, and major depressive disorders (MDD) contribute to a significant heavy disease burden, which is expected to be second by 2050, only to heart disease. Despite great improvement in therapy, the treatment efficacy remains low. Therefore, alternative therapies have been intensely investigated. A substantial body of researches have suggested that inflammation is one of the operative pathways between MDD and increased risk of somatic comorbidities, and some specific depressive symptoms. Depression occurs in most patients with cardiac and cerebrovascular disease due to the long-term effects, and depression increases the risk of cardiovascular disease in the population as a whole and in patients with coronary artery disease or stroke. Several observational studies have demonstrated reduced rates of depression among patients taking statins, which may be related to its anti-inflammatory effect. However, whether statin improves the depressive symptoms and its associated mechanism is still mixed. Furthermore, there is little evidence about statin treatment effect in those with moderate to severe depression. In addition, whether the effect of statin treatment on depressive symptom changes with time or is affected by baseline depression severity or percentage change of lipid levels has not been explored in previous studies.
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Cui, Chaohua, Ning Chen, Shuju Dong, and Li He. Statin Pretreatment Combined With Intravenous Thrombolysis for Ischemic Stroke Patients: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0047.

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Liu, Xueyong. Associations between statin use and osteoarthritis risk and progression: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0160.

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Zhao, Fangfang, Chunli Lu, Luying Chen, Yaxin Guo, Lijie Lu, Yuerong Jiang, Jianping Liu, and Keji Chen. Red yeast rice preparations for dyslipidemia: A protocol for an overview of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0032.

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Review question / Objective: What is the quality of systematic reviews/meta-analysis of red yeast rice (RYR) preparations for dyslipidemia? What is the comparative benefit of red yeast rice preparations on dyslipidemia compared to other lipid-lowering drugs? Based on the current controversies in dyslipidemia guidelines and clinical practice, to explore the relative benefits of red yeast rice compared with other lipid-lowering drugs, we plan to perform an overview of existing SRs/MAs. Condition being studied: Red yeast rice (RYR) has been used as an alternative to statin therapy in treating patients with dyslipidemia, particularly in those considered to be statin intolerant due to statin-associated myalgia (SAM), and clinical studies suggest that RYR is well-tolerated, safe, and effective for cardiovascular disease (CVD) primary prevention. Several studies support the beneficial effect of RYR on blood lipid profiles. Dyslipidemia is a worldwide public health challenge because of its high prevalence, leading to significant economic and social burdens. Many systematic reviews (SRs) /meta-analysis (MAs) have been performed to prove the effects of RYR on dyslipidemia during the past several years. High-quality SRs/MAs can provide clinicians, patients, and other decision-makers with a reliable scientific basis. However, existing SRs/MAs showed varied and heterogeneous results.
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Huang, Hao, Hechen Zhu, and Ru Ya. Statin use in older people primary prevention on cardiovascular disease: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0045.

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Niu, Xiaowei, and Shuwen Hu. Efficacy and safety of PCSK9 inhibitors and statin lipid-lowering therapy in coronary atherosclerosis: A meta-analysis of randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0019.

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Martini, L., G. Swallow, G. Heron, and M. Bocci. Pseudowire Status for Static Pseudowires. RFC Editor, May 2012. http://dx.doi.org/10.17487/rfc6478.

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Carver-Thomas, Desiree, and Susan Patrick. Understanding Teacher Compensation: A State-by-State Analysis. Learning Policy Institute, April 2022. http://dx.doi.org/10.54300/443.847.

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Offering competitive teacher compensation is an important part of the puzzle to recruiting and retaining a strong and diverse teacher workforce. The maps and associated tables that follow show three teacher wage indicators for each state: (1) average annual starting salary for public school teachers, (2) average annual starting salary for public school teachers adjusted for cost-of-living differences across states, and (3) average weekly wage competitiveness—how much teachers earn relative to other college-educated workers in that state. Together, these indicators signal the overall wage conditions underlying efforts to attract and retain well-prepared teachers across a state. The final table in the series shows all three indicators for each state. Teacher starting salaries and cost of living vary by district, so within states (with the exception of Hawaii and Washington, DC, which each comprise a single school district), there are districts that will be higher or lower than their state average on these indicators.
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Crawford, Jennifer. United States Navy Advanced Crew Station Evaluation Techniques. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada377911.

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Hunter, Margaret, Jijo K. Mathew, Ed Cox, Matthew Blackwell, and Darcy M. Bullock. Estimation of Connected Vehicle Penetration Rate on Indiana Roadways. Purdue University, 2021. http://dx.doi.org/10.5703/1288284317343.

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Over 400 billion passenger vehicle trajectory waypoints are collected each month in the United States. This data creates many new opportunities for agencies to assess operational characteristics of roadways for more agile management of resources. This study compared traffic counts obtained from 24 Indiana Department of Transportation traffic counts stations with counts derived by the vehicle trajectories during the same periods. These stations were geographically distributed throughout Indiana with 13 locations on interstates and 11 locations on state or US roads. A Wednesday and a Saturday in January, August, and September 2020 are analyzed. The results show that the analyzed interstates had an average penetration of 4.3% with a standard deviation of 1.0. The non-interstate roads had an average penetration of 5.0% with a standard deviation of 1.36. These penetration levels suggest that connected vehicle data can provide a valuable data source for developing scalable roadway performance measures. Since all agencies currently have a highway monitoring system using fixed infrastructure, this paper concludes by recommending agencies integrate a connected vehicle penetration monitoring program into their traditional highway count station program to monitor the growing penetration of connected cars and trucks.
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