Thematische Bibliographien / Atherosclerosis Drugs

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Auswahl der wissenschaftlichen Literatur zum Thema „Atherosclerosis Drugs“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 1. Februar 2022

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Zeitschriftenartikel zum Thema "Atherosclerosis Drugs"

Udupa, S. L. „Indigenous drugs and atherosclerosis“. Drugs of Today 37, Nr. 1 (2001): 37. http://dx.doi.org/10.1358/dot.2001.37.1.608780.

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Orekhov, Alexander N., Gregory N. Baldenkov, Vladimir V. Tertov, Li Hwa Ryong, Sergei G. Kozlov, Anatoly A. Lyakishev, Vsevolod A. Tkachuk, Michael Ya Ruda und Vladimir N. Smirnov. „Cardiovascular Drugs and Atherosclerosis“. Journal of Cardiovascular Pharmacology 12, Supplement 6 (1988): S66—S68. http://dx.doi.org/10.1097/00005344-198812006-00017.

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Bruikman, Caroline S., Robert M. Stoekenbroek, G. Kees Hovingh und John P. Kastelein. „New Drugs for Atherosclerosis“. Canadian Journal of Cardiology 33, Nr. 3 (März 2017): 350–57. http://dx.doi.org/10.1016/j.cjca.2016.09.010.

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Cao, Qi, Jiarui Zhao, Maochen Xing, Han Xiao, Qian Zhang, Hao Liang, Aiguo Ji und Shuliang Song. „Current Research Landscape of Marine-Derived Anti-Atherosclerotic Substances“. Marine Drugs 18, Nr. 9 (25.08.2020): 440. http://dx.doi.org/10.3390/md18090440.

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Atherosclerosis is a chronic disease characterized by lipid accumulation and chronic inflammation of the arterial wall, which is the pathological basis for coronary heart disease, cerebrovascular disease and thromboembolic disease. Currently, there is a lack of low-cost therapeutic agents that effectively slow the progression of atherosclerosis. Therefore, the development of new drugs is urgently needed. The research and development of marine-derived drugs have gained increasing interest from researchers across the world. Many marine organisms provide a rich material basis for the development of atherosclerotic drugs. This review focuses on the latest technological advances in the structures and mechanisms of action of marine-derived anti-atherosclerotic substances and the challenges of the application of these substances including marine polysaccharides, proteins and peptides, polyunsaturated fatty acids and small molecule compounds. Here, we describe the theoretical basis of marine biological resources in the treatment of atherosclerosis.

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Moubayed, Sami P., Therese M. Heinonen und Jean-Claude Tardif. „Anti-inflammatory drugs and atherosclerosis“. Current Opinion in Lipidology 18, Nr. 6 (Dezember 2007): 638–44. http://dx.doi.org/10.1097/mol.0b013e3282f0ee11.

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Evangeline, Seth, und Priya R. Iyer. „Atherosclerosis: Causes and Cures“. Healthcare Review 2, Nr. 1 (05.08.2021): 34–44. http://dx.doi.org/10.47285/hr.v2i1.87.

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Atherosclerosis is a systemic disease that occurs due to the formation of Fibro-fatty lesions in arteries that block blood flow. The process of Atherosclerosis is initiated through mechanical, chemical, and immunological activation of the endothelium. Even there are microorganisms involved in the different stages of atherosclerosis. There are a number of molecular factors, RNA’s, macrophages and enzymes that play a vital role in the progression and development of Atherosclerosis that alter the metabolism of Fibro-fatty. Receptors of micro RNA proliferate and regulate endothelial activation and smooth cell Macrophages, monocytes, t-cell and natural killer cells involved in the boosting of the immune system to prevent the atherosclerotic lesion formation. In this review, we can know how RNA’s involved in the pathophysiology side of atherosclerosis and explore the mechanism to regulate Atherosclerosis, and how macrophages evoke an immune response. Therefore, the use of synthetic and natural drugs and following the right diet timely prevent and reduce the risk of development of Atherosclerosis.

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Boskovic, Srdjan, und Aleksandar Neskovic. „Atherosclerosis plaque regression“. Medical review 59, Nr. 1-2 (2006): 38–45. http://dx.doi.org/10.2298/mpns0602038b.

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Introduction. The natural history of atherosclerosis can be assessed using different methods including quantitative coronary angiography, intravascular ultrasound, B-mode ultrasound, electron-beam computed tomography and magnetic resonance imaging. Regression of atherosclerosis. Although the first investigations regarding effects of low cholesterol diet on atherosclerosis progression in animals were performed almost 100 years ago, researches on potential induction of atherosclerosis regression in humans began only recently, in the past 20 years. To date, many studies assessing different drugs and study protocols on natural evolution of atherosclerosis have been performed. They include use of diet and physical activity, different hypolipemic drugs, especially statins, ACE inhibitors, calcium channel blockers, hormone replacement therapy, antioxidants, and recently, use of recombinant apolipoproteins. Statins and atherosclerosis. It has been established that statins given to patients with, or even without verified coronary artery disease, slow progression of atherosclerosis. These effects of statins are likely due to a combination of their metabolic and pleiotropic properties and might in part explain the positive effects of these drugs on overall cardiovascular mortality and morbidity. Furthermore, applied in high doses, these drugs may induce real atherosclerosis regression, especially in asymptomatic patients in the early stages of the disease. .

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Skripnikova, I. A., O. V. Kosmatova, M. A. Kolchinа, M. A. Myagkova und N. A. Alikhanova. „Atherosclerosis and Osteoporosis. Common Targets for the Effects of Cardiovascular and Anti-Osteoporotic Drugs (Part II). The Effect of Antiosteoporotic Drugs on the Vascular Wall State“. Rational Pharmacotherapy in Cardiology 15, Nr. 3 (06.07.2019): 359–67. http://dx.doi.org/10.20996/1819-6446-2019-15-3-359-367.

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In the second part of the literature review, data are presented on the possible effect of anti-osteoporosis therapy on the vascular wall and the development of calcification. The discovery of common biological substances involved in the development of atherosclerosis, calcification of the vascular wall and osteoporosis attracts the attention of scientists in terms of targets for assessing the effects of already known drugs or developing new drugs that can simultaneously prevent or slow the progression of both atherosclerosis and osteoporosis. Currently, various groups of drugs for the treatment of osteoporosis have been studied to prevent or reduce the progression of subclinical atherosclerosis and calcification. Both antiresorptive drugs (bisphosphonates, monoclonal antibodies to RANKL, selective estrogen receptor modulators), and bone-anabolic therapy, which includes teriparatide, were studied. However, there are a few such studies and the most promising drugs that have a preventive effect in the early stages of atherosclerotic damage are bisphosphonates. Other classes of antiosteoporotic drugs did not reveal a positive effect on the vascular wall, and some of them increased the cardiovascular risk. Divergences in the results of experimental and clinical studies attract attention. If in the experiment almost all drugs for the treatment of osteoporosis had an atheroprotective effect and suppressed vascular calcification, then in clinical conditions only bisphosphonates confirmed the positive effect on the vascular wall.

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Berman, Jeremy P., Michael E. Farkouh und Robert S. Rosenson. „Emerging anti-inflammatory drugs for atherosclerosis“. Expert Opinion on Emerging Drugs 18, Nr. 2 (16.05.2013): 193–205. http://dx.doi.org/10.1517/14728214.2013.801453.

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Gallego-Colon, Enrique, Wojciech Wojakowski und Tomasz Francuz. „Incretin drugs as modulators of atherosclerosis“. Atherosclerosis 278 (November 2018): 29–38. http://dx.doi.org/10.1016/j.atherosclerosis.2018.09.011.

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Dissertationen zum Thema "Atherosclerosis Drugs"

Layne, Kerry Anne. „Anti-inflammatory effects of anti-platelet drugs : implications for atherosclerosis“. Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/antiinflammatory-effects-of-antiplatelet-drugs(1da58105-e415-4241-a696-effb35badd21).html.

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Cardiovascular disease secondary to atherosclerosis is the leading cause of death worldwide. The pathophysiology of atherosclerosis is multifactorial and complex. This thesis offers insight into the regulation of several potential biomarkers of cardiovascular disease and explores the effects of anti-platelet therapy in modulating these pathways. CD14highCD16+ monocytes are elevated in patients with atherosclerosis and may be predictive of future cardiovascular events. The initial study in this PhD project assessed the effects of anti-platelet drugs on the phenotype of circulating monocytes in 60 healthy volunteers in the presence of mild, systemic inflammation induced by the influenza immunisation. A significant rise in circulating CD14highCD16+ monocytes developed following immunisation and anti-platelet therapy was subsequently shown to exert an immunomodulatory action by counteracting this response. Netrin-1 is a laminin-like protein that is implicated in cardiovascular disease, including coronary artery disease. A series of experiments were performed to investigate the biomolecular mechanisms that regulate the synthesis of vascular netrin-1 in humans. Results showed that netrin-1 levels are directly modulated by changes in the production of vasoactive cyclooxygenase-derived molecules, such as prostaglandin E2, from the vascular endothelium. Oxidised low-density lipoprotein was the final biomarker that was investigated. Results indicated that CD16+ monocytes may regulate the clearance of oxidised lipoproteins and their systemic accumulation, possibly through the internalisation of circulating oxLDL/IgG immunocomplexes mediated by Fc γ receptors, including CD16.

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Roberts, Ladeidra Monet. „ANTIRETROVIRAL DRUGS EFAVIRENZ AND TENOFOVIR AND THEIR EFFECTS ON ARTERIAL REMODELING AND PROTEASE ACTIVITY“. Thesis, Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53731.

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Highly antiretroviral therapies (HAART) have been implemented to slow the progression of the human immunodeficiency virus (HIV). Although these new advances in the medications for HIV-positive patients have contributed in longer life expectancy, comorbidities, such as cardiovascular disease, still cause higher number of deaths among HIV-positive patients than in the regular population. Because of the intrinsic inflammation caused by the HIV virus, atherogenesis is more likely to occur and is driven by infected macrophages. These macrophages are known to secrete cathepsins, but infection causes the macrophages not to perform their function properly as an immune agent. I hypothesize that antiretroviral drugs play an important role in arterial remodeling by affecting cells within the artery and causing an alteration of cathepsin activity, leading to an increased risk of atherosclerosis in HIV patients. To test this hypothesis, we incubated THP-1 monocytes with antiretroviral drugs efavirenz and tenofovir individually to observe any changes in cathepsin activity. These lysates were analyzed through multiplex cathepsin zymography and quantified through densitometry. We found that our hypothesis held true for efavirenz and tenofovir in THP-1 monocytes, which caused decreased cathepsin K activity compared to vehicle controls. Still, stimulation of peripheral blood mononuclear cells (PBMCs) with efavirenz and tenofovir caused differential effects. Together, our data suggest that the HAART interaction with monocytes that are physiologically relevant to our system possibly contributes to the advancement of atherogenesis in HIV+ patients.

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Yan, Y. (Ying). „The antichlamydial effects of drugs used in cardiovascular diseases“. Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514293153.

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Abstract Chronic Chlamydia pneumoniae infections have been associated with cardiovascular diseases (CVD), but the treatment is difficult. Some drugs used for CVD have been found to have an inhibitory effect on the C. trachomatis infection, which is not considered to be associated with CVD. The purpose of this study was to investigate the effects of heparan sulfate-like glycosaminoglycans, COX inhibitors and rapamycin on the C. pneumoniae infection with cell culture methods. Almost any conceivable factors may affect the results of cell cultures. This study showed the complex interaction between temperature, time and medium during the pre-treatment before inoculation. The influences of these factors on the results overlapped and interlaced. The simple washing procedure could enhance the infectivity of C. pneumoniae although it is generally considered to cause the loss of chlamydial EBs and sequentially decrease the chlamydial infectivity. Although the detailed mechanisms were not studied, the results of this study showed that selective COX inhibitors and rapamycin can inhibit the infectivity of C. pneumoniae by inhibiting the growth and maturation, whereas heparan sulfate-like glycosaminoglycans perhaps inhibit the attachment of C. pneumoniae EBs onto the host cells. Recovery and repassage results showed that the growth can be only delayed by selective COX inhibitors, and it can recover to normal level once the drugs were removed. However, rapamycin inhibited the maturation of chlamydial EBs and therefore the infectivity fell down further even when the rapamycin was removed. This study also presented the variations of pathogenicity between different C. pneumoniae strains in vitro. This study is based on in vitro experiments with an acute infection model. Thus, any definite conclusions on the possible antichlamydial effects of the drugs tested in the treatment of cardiovascular diseases which are associated with chronic C. pneumoniae infections cannot be drawn on the basis of this study.

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Hansen, Laura Marie. „Mechanical and structural effects of HIV-1 proteins and highly active antiretroviral therapy (HAART) drugs on murine arteries“. Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/45791.

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The overall goals of this project were to develop microstructurally based constitutive models to characterize the mechanical behavior of arteries and to investigate the effects of HIV proteins and antiretroviral drugs on the microstructure and mechanical behavior. To this end we created several constitutive models in aim 1 using a rule of mixtures approach, investigated the role of viral proteins in aim 2 through the use a transgenic mouse model, and studied the effects of the antiretroviral drug AZT administered to mice in aim 3. It is well known that the local mechanical environment which cells experience mediates growth and remodeling and that subsequent growth and remodeling can change that mechanical environment. This remodeling includes changes in the content and organization of the constituents of arteries (collagen, elastin, and smooth muscle cells). The first aim thus created models that incorporated the content and organization of these constituents using a rule-of-mixtures approach. The models we developed were able to capture the mechanical behavior of the arteries as well as previously developed phenomenological models while providing more physical meaning to the parameters, some which can be measured experimentally for incorporation into future models. Aims 2 and 3 investigated the mechanical and microstructural changes to murine arteries in response to HIV proteins or the drug AZT. While the development of antiretroviral therapy has greatly increased the life expectancy of patients with HIV, a number of other complications and co-morbidities including cardiovascular disease have become apparent. While clinical data has implicated both the virus and the antiretroviral drugs as playing roles, this work addressed the need of investigating these effects in a controlled manner. Specifically we used mouse models and focused on the two subclinical markers of increased intima-media thickness and arterial stiffening. Aim 2 used a transgenic mouse that expressed most of the human HIV proteins. We observed both intima-media thickening and arterial stiffening in alignment with clinical data. Other changes that also support a proatherogenic phenotype included decreased elastin content and changes in cathepsin activity. Aim 3 administered the antiretroviral drug AZT to healthy mice and we also observed the same subclinical markers of atherosclerosis including intima-media thickening and arterial stiffening as well as the other proatherogenic changes of decreased elastin and changes in cathepsin activity. Several other parameters including axial behavior, opening angles, collagen content, and collagen fiber angles were also quantified. These were important to fully characterize the vessel and may also be incorporated in the future into the constitutive models developed in aim1. In conclusion, in aim 1 we developed a microstructurally based constitutive model of arteries that effectively captures the mechanical behavior and includes parameters that have more physical meaning and some of which are experimentally tractable. Aims 2 and 3 both observed several subclinical markers of atherosclerosis in mice that express HIV proteins or were given AZT, providing a good model for future work and suggesting that both the HIV virus and antiretroviral drugs may play roles in the development of atherosclerosis in HIV.

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Li, Yu-I. „Is tanshinone IIA, the active ingredient of Chinese herbal supplement danshen, really beneficial? : a study from cell and animal perspectives /“. Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/6603.

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Vitório, Tatiana Solano. „Paclitaxel e metotrexato associados a uma nanoemulsão lipídica no tratamento da aterosclerose em coelhos“. Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-26032010-110559/.

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Em estudos anteriores, mostramos que uma nanoemulsão artificial (NEm) de composição semelhante à da lipoproteína de baixa densidade se liga a receptores de lipoproteínas de baixa densidade após sua injeção na corrente sanguínea. Como tais receptores estão superexpressos em células com altas taxas de proliferação, como ocorre no cancer e na aterosclerose, a NEm pode ser utilizada como veículo para direcionar drogas a estas células, diminuindo sua toxicidade e aumentando sua ação farmacológica. Recentemente, reportamos que a associação de um derivado do agente antiproliferativo paclitaxel, o oleato de paclitaxel (OPTX) à NEm reduziu em 60% a área lesionada de aortas de coelhos submetidos à dieta rica em colesterol. Neste estudo, testamos o efeito sinérgico da terapia combinada do OPTX-NEm com um derivado do metotrexato, o di-dodecil metotrexato (DMTX), também associado à NEm. O MTX, além de sua ação antiproliferativa, também possui propriedades imunossupressoras. Coelhos machos da raça Nova Zelândia foram submetidos à dieta enriquecida com 1% de colesterol durante 8 semanas. A partir da quinta semana de consumo da dieta, 8 animais foram injetados semanalmente com solução salina por via endovenosa (grupo controle) e 8 receberam o tratamento combinado de OPTX-NEm (4mg/Kg) com DMTX-NEm (4mg/Kg), por 4 semanas. Ao final das 8 semanas, os animais foram sacrificados. As aortas dos animais foram retiradas, abertas longitudinalmente, fixadas em formalina tamponada a 10% e coradas com Escarlate R para a análise macroscópica da lesão. Os arcos aórticos foram seccionados em fragmentos de 5mm, embebidos em parafina e os cortes realizados foram corados com hematoxilina-eosina, para a determinação da área das camadas íntima e média. O tratamento combinado de OPTX-NEm com DMTX-NEm reduziu a área das lesões em 82%, em comparação ao grupo controle, e a razão da área da lesão/área total diminuiu de 0,82±0,08 para 0,08±0,06 (p<0,01). Por meio das avaliações da variação do consumo de ração, peso corporal e contagem de leucócitos totais (p>0,05), pode-se afirmar que os tratamentos não apresentaram toxicidade significativa, exceto pela queda na contagem de eritrócitos (p<0,05). Como conclusão, a quimioterapia combinada de OPTX e DMTX associados à NEm como veículo mostrou-se eficaz na redução da área de lesão aterosclerótica em coelhos e a toxicidade relacionada aos fármacos foi nitidamente reduzida.
In previous studies we have shown that an artificial nanoemulsion (NEm) that resemble LDL composition are taken-up by LDL receptors after injection into the bloodstream. As those receptors are upregulated in cells with higher proliferation rates, as occurs in cancer and atherosclerosis, NEm can be used as vehicle to direct drugs against those cells, diminishing toxicity and increasing pharmacological action. Recently, we reported that association of antiproliferative agent paclitaxel derivative, paclitaxel oleate (OPTX) to NEm reduced by 60% the lesion area of cholesterol-fed rabbits. In this study, the combined chemotherapy of OPTX-NEm with a methotrexate derivative, di-dodecil methotrexate (DMTX), also associated with NEm, was tested for synergistic effects. MTX, besides antiproliferative action, has also immunosuppressant properties. Male New Zealand rabbits were fed a 1% cholesterol diet for 60 days. Starting from day 30, 8 animals were treated with 4 weekly I.V. saline solution injections (control group) and 8 with combined OPTX-NEm (4 mg/kg) plus DMTX-NEm (4 mg/kg) for additional 30 days. On day 60, the animals were sacrificed for analysis. Aorta was excised, open longitudinally, placed in 10% buffered formalin and stained in Scarlet R for lesion macroscopic analysis. Segments of 5mm of the aortic arch were embedded in paraffin and sections were taken and stained in hematoxylin-eosin for intima and media area measurement. In comparison with controls, treatment with combined OPTX-NEm plus DMTX-NEm reduced the lesion area by 82% and the lesion/total area ratio was decreased from 0,82±0,08 to 0,08±0,06 (p<0.01). Except for decrease in erythrocyte count (p<0.05), treatments were devoid of significant toxicity, as evaluated by food intake, body weight and leucocyte count (p>0.05). In conclusion, this novel approach consisting in combined chemotherapy of OPTX and DMTX using NEm as a drug-targeting vehicle showed effective lesion area regression in rabbits and marked toxicity reduction.

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Vukmirovic, Neda. „Drug deposition and distribution in healthy and atherosclerotic arteries and in models of atherosclerosis following bulk or stent-based drug delivery“. Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/40871.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2007.
Includes bibliographical references.
Drug eluting stents have revolutionized the practice of medicine and the landscape of medical devices. Yet, more than four years after introduction clinical trial data and clinical use have still not fully clarified what drives the safety and efficacy of these devices. The goal of this thesis was to help fill this void by describing the mechanisms by which stent-eluted drugs are distributed within healthy and atherosclerotic vascular models. In the first part of the thesis we investigated the effect of drug physicochemical properties on drug deposition, retention, and distribution in a healthy vascular model. We found that hydrophobic drugs are deposited to a far greater degree than hydrophilic drugs, with longer retention times, and distribution patterns that likely track with specific and general binding sites. The second part of the thesis investigated how arterial ultrastructure in health and disease modulates the arterial deposition and distribution of hydrophobic antiproliferative drugs used with drug-eluting stents. We tracked the distribution of radiolabeled and FITC-labeled compounds and demonstrated that macrostructural changes in arterial architecture led to profound changes in drug deposition. Paclitaxel in particular was sensitive to tissue state.
(cont.) This drug binds specifically to tubulin and to lesser extent in a general manner to elastic. Drug levels fell as paclitaxel, tubulin and elastin were displaced by lipid and collagen. These observations might well explain how drugs may partition within different arterial lesions as determined by lesion composition. Finally, we demonstrated that association with these binding sites was governed by association kinetics that reflects the different components of the arterial wall compartments. Slower release kinetics yielded up to 64% higher deposition of a drug from stents implanted in rabbit iliac arteries over a 28-day period. Mathematical modeling illustrates that the dependence of drug deposition on stent release kinetics is contingent on drug retention. Further model development is implicated for predicting drug deposition profiles for different types of drugs, arterial states, and stent release kinetics.
by Neda Vukmirovic.
Ph.D.

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Soubhye, Jalal. „Design, synthesis and study of myeloperoxidase inhibitors in the series of 3-alkylindole“. Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209402.

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The deleterious effects of MPO make it a new target for medicinal research. The aim of our study is to find promising inhibitors of MPO for using them as starting point of new anti-inflammatory drugs. Depending on previous researches on MPO inhibitors, we selected 5-fluorotryptamine as starting compounds. Using docking experiments, we designed a series of compounds derived from 5-fluorotryptamine. Two modifications were proposed:

&
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Deosarkar, Sudhir P. „Development of Novel Therapeutic and Diagnostic Approaches for Atherosclerosis“. Ohio University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1268371885.

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Fulmer, Makenzie L., Emilee Englehaupt, Chris Garst und Stacy D. Brown. „Type 2 Cannabinoid Receptor Deficiency is Associated with Atherosclerotic Lesion Calcification in Ldr-null Mice“. Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/5271.

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Background: Calcification of atherosclerotic plaques is associated with vulnerability to rupture and increased risk of myocardial infarction. The mechanism of plaque calcification is unclear, but has been shown to be a cell-mediated process involving complex signaling pathways affecting the osteogenic transcription factor Runt-related transcription factor 2 (Runx2). The type-2 cannabinoid receptor (CB2) modulates processes involved in bone remodeling and our prior studies determined that CB2 alters the composition of early lesions in hyperlipidemic Ldlr-/- mice; however, the function of CB2 in plaque calcification is unknown. Therefore, we tested the hypothesis that CB2 modulates plaque calcification by evaluating the effects of systemic CB2 gene deletion on lesion calcification and aortic expression of Runx2 in Ldlr-/- mice. Results: Groups (n≥8) of 8-week old CB2+/+Ldlr-/- (WT) and CB2-/- Ldlr-/- (CB2-/-) mice were fed a high fat diet (HFD) for up to 24 weeks. Standard blood plasma analysis showed no difference in HFD-induced hyperlipidemia between WT and CB2-/- mice. Aortic levels of endocannabinoids, anandamide and 2-archidonylglycerol, were significantly elevated after 12 weeks of HFD feeding as determined by LC-MS/MS. En face analysis revealed the extent of atherosclerosis in the aortic arch and thoracic aorta did not differ between WT and CB2-/- mice, but was ~1.9-fold greater in the abdominal aortas of CB2-/- mice (17.0±1.3% vs 9.0±1.3%, p=0.002). Calcification of aortic root lesions was ~2.3 fold greater in CB2-/- mice compared to WT mice (12.9±1.1% vs 5.6±1.2%, p=0.002) as revealed by von Kossa staining. Western blot analysis showed significantly increased expression of Runx2 in aortas of WT mice compared to CB2-/- after 20 weeks of HFD (2.55±0.25 fold, p Conclusion: Systemic CB2 deficiency enhances lesion calcification and is associated with altered aortic expression of Runx2. These results provide novel mechanistic insights into the function of CB2 signaling in the pathogenesis of atherosclerosis and vascular calcification that may lead to the development of therapies aimed at stabilizing calcified plaque.

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Bücher zum Thema "Atherosclerosis Drugs"

von Eckardstein, Arnold, Hrsg. Atherosclerosis: Diet and Drugs. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0.

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International Symposium on Drugs Affecting Lipid Metabolism (8th 1983 Philadelphia, Pa.). Drugs affecting lipid metabolism VIII. New York: Plenum Press, 1985.

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Cholesterol and atherosclerosis: Diagnosis and treatment. Philadelphia: Lippincott, 1990.

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Morton, Walker, Hrsg. Chelation therapy: The key to unclogging your arteries, improving oxygenation, treating vision problems, reversing sexual difficulties, fighting arthritis, an alternative to amputation. Greenwich, Conn: Devin-Adair, 1985.

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Brecher, Harold. Forty something forever: A consumer's guide to chelation therapy. Herndon, Va: Healthsavers Press, 1992.

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Brecher, Harold. Forty something forever: A consumer's guide to chelation therapy and other heart-savers. Herndon, VA: Healthsavers Press, 1999.

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The cholesterol wars: The skeptics vs. the preponderance of evidence. San Diego, Calif: Academic Press, 2007.

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Steinberg, Daniel. The cholesterol wars: The skeptics vs. the preponderance of evidence. San Diego, Calif: Academic Press, 2007.

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Steinberg, Daniel. The cholesterol wars: The skeptics vs. the preponderance of evidence. San Diego, Calif: Academic Press, 2007.

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Bypassing bypass: The new technique of chelation therapy : a non-surgical treatment for improving circulation and slowing the aging process. 2. Aufl. Trout Dale, VA: Medex Publishers, 1996.

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Buchteile zum Thema "Atherosclerosis Drugs"

Stein, Evan A. „Lipid-Lowering Drugs“. In Atlas of Atherosclerosis, 165–91. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4615-6484-3_9.

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Hunninghake, Donald B., und Evan A. Stein. „Lipid-Lowering Drugs“. In Atlas of Atherosclerosis, 155–77. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4757-9310-9_9.

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Steiner, George. „Diabetes and Atherosclerosis: The Diabetes Atherosclerosis Intervention Study (Dais)“. In Drugs Affecting Lipid Metabolism, 405–11. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_47.

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Avogaro, P., G. Bittolo Bon und G. Cazzolato. „Phospholipids in Human Atherosclerosis“. In Drugs Affecting Lipid Metabolism, 407–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_77.

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Lees, Robert S., Ann M. Lees, John Lister-James und Richard T. Dean. „Radiopharmaceutical Imaging of Atherosclerosis“. In Drugs Affecting Lipid Metabolism, 119–24. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_13.

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Cullen, P., J. Rauterberg und S. Lorkowski. „The Pathogenesis of Atherosclerosis“. In Atherosclerosis: Diet and Drugs, 3–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0_1.

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Clair, R. St, und M. Anthony. „Soy, Isoflavones and Atherosclerosis“. In Atherosclerosis: Diet and Drugs, 301–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0_10.

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Mandal, K., M. Jahangiri und Q. Xu. „Autoimmune Mechanisms of Atherosclerosis“. In Atherosclerosis: Diet and Drugs, 723–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0_27.

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Vähäkangas, E., und S. Ylä-Herttuala. „Gene Therapy of Atherosclerosis“. In Atherosclerosis: Diet and Drugs, 785–807. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0_30.

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Harker, L. A. „Animal Models Evaluating Platelet-Modifying Drugs“. In Platelets and Atherosclerosis, 25–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-58225-7_4.

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Konferenzberichte zum Thema "Atherosclerosis Drugs"

Sarker, Sunandita, Yiannis S. Chatzizisis, Srivatsan Kidambi und Benjamin S. Terry. „Design and Development of a Novel Drug Delivery Catheter for Atherosclerosis“. In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6869.

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Atherosclerosis is a chronic progressive cardiovascular disease that results from plaque formation in the arteries. It is one of the leading causes of death and loss of healthy life in modern world. Atherosclerosis lesions consist of sub-endothelial accumulations of cholesterol and inflammatory cells [1]. However, not all lesions progress to the final stage to cause catastrophic ischemic cardiovascular events [2]. Early identification and treatment of high-risk plaques before they rupture, and precipitate adverse events constitutes a major challenge in cardiology today. Numerous investigations have confirmed that atherosclerosis is an inflammatory disease [3] [4] [5]. This confirmation has opened the treatment of this disease to many novel anti-inflammatory therapeutics. The use of nanoparticle-nanomedicines has gained popularity over recent years. Initially approved as anticancer treatment therapeutics [6], nanomedicine also holds promise for anti-inflammatory treatment, personalized medicine, target-specific treatment, and imaging of atherosclerotic disease [7]. The primary aim of this collaborative work is to develop and validate a novel strategy for catheter-directed local treatment of high-risk plaque using anti-inflammatory nanoparticles. Preselected drugs with the highest anti-inflammatory efficacy will be incorporated into a novel liposome nanocarrier, and delivered in-vivo through a specially designed catheter to high-risk atherosclerotic plaques. The catheter has specially designed perfusion pores that inject drug into the blood stream in such a controlled manner that the streamlines carry the nanoparticles to the stenotic arterial wall. Once the particles make it to the arterial wall, they can be absorbed into the inflamed tissue. In this paper, we discuss the design and development of an atraumatic drug delivery catheter for the administration of lipid nanoparticles.

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Nishizawa, E. E., und D. J. Williams. „PERIVASCULAR CAROTID ARTERY INJURY LEAD TO ATHEROSCLEROSIS IN HYPERCHOLESTEROLEMIC RABBITS“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643085.

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We have previously shown that endothelial injury results when clotted blood is placed perivascularly around a rabbit carotid artery. This injury was manifested by loss of endothelial cells and adherence of leukocytes and platelets. When similar injury was induced in hypercholesterolemic rabbits, medial lesions as well as intimal proliferation was observed. We have extended these studies and have found that these lesions contain high concentrations of cholesterol (200-300 mg/gm protein compared to 40-80 mg/gm protein in controls) suggesting lipid infiltration. The uniformity of lipid accumulation along the injured tissue segment, which was measured as intimal thickening of serial sections, suggests that these lesions are not focal and that the injury was initiated by the perivascular blood rather than by mechanical injury. The contralateral non-injured vessels showed no lesions (0-2% of the total intima + media area) and normal cholesterol content. When the serum cholesterol level was decreased from about 1200 mg/dl to 450 mg/dl by use of drugs such as Colestid, the intimal proliferation was 8.9% compared to the untreated controls, which were around 36%. Aspirin, which did not lower serum cholesterol, had no effect on intimal proliferation and arterial cholesterol accumulation. These studies suggest that this model might be useful for evaluating antiatherosclerotic drugs.

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Tristantini, Dewi, M. Rizki Ramadhan und Aisyah Hanifah. „Shelf life estimation of anti-atherosclerosis herbs using ASLT: Critical water content and sorption isotherms model“. In THE 4TH BIOMEDICAL ENGINEERING’S RECENT PROGRESS IN BIOMATERIALS, DRUGS DEVELOPMENT, HEALTH, AND MEDICAL DEVICES: Proceedings of the International Symposium of Biomedical Engineering (ISBE) 2019. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5139350.

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SEIFFGE, D., und U. Weithmann. „SURPRISING EFFECTS OF THE CONSECUTIVE ADMINISTRATION OF PENTOXIFYLLINE AND LOW DOSE ACETYLSALICYLIC ACID ON THROMBUS FORMATION.“ In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643444.

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The effect of the combined oral administration of pentoxifylline (pof) and low dose acetylsalicylic acid (ASA) was evaluated with the help of the laser-induced thrombosis model in rat mesenteric arterioles. Laser-induced thrombosis is inhibited in a dose-dependent way by both drugs. The administration of ASA, either simultaneously with or 1 hour prior to pof, does not show any effects in the laser model. On the contrary, the administration of pof followed 1 h later by ASA not onyl exhibited a significant effect but also produced a supraadditive inhibition of the laser-induced thrombus formation. Specific investigations concerning the time interval between the administration of both drugs determined that a significant effect can be achieved only after an interval of 30 to 90 minutes (principle of HWA 5112).The striking results could also be shown in diseased animals after consecutive chronic administration of pof 1 h prior to ASA. HWA 5112 exhibits significant effects on laser-induced thrombus formation in the following chronic animal models: 1. adjuvant arthritic rats, 10 → 1 mg/kg for 21 days; 2. spontaneously hypertensive stroke-prone rats, 10→ 1 mg/kg three times within 24 h; 3. cholesterol-induced atherosclerosis in rabbits, 10→ 1 mg/kg for 14 days. The reported data clearly demonstrate that the sequential drug administration of first pentoxifylline followed 30 to 90 min later by ASA exhibits a supraadditive antithrombotic effect.

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Klein-Soyer, C., F. Driot, J. L. Vonesch, A. Beretz, J.-P. Maffrand, J.-p. Cazenave und E. Wittendorp-Rechenmann. „MODULATION BY HEPARINS OR PENTOSAN POLYSULFATE OF THE EFFECTS OF ACIDIC AND BASIC HUMAN FIBROBLAST GROWTH FACTORS (aFGF and bFGF) ON THE REPAIR OF A MECHANICAL LESION OF THE ENDOTHELIUM“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643358.

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A mechanical injury to endothelium (EC) may be followed by vascular spasm, platelet adhesion to exposed subendothelium, mural thrombosis and atherosclerosis. Heparin (HEP) can protect EC from injury, inhibits smooth muscle cells proliferation and has been proposed in the treatment of atherosclerosis. aFGF and bFGF are potent mitogens for EC in vitro and angiogenic in vivo. HEP increases the growth promoting activity of aFGF in EC culture. We have studied the effects of HEP (Choay), low molecular weight HEP (LMWH, CY216 Choay) or pentosan poly sulfate (PPS, Clin-Midy) in the presence of aFGF or bFGF on the repair process, after a mechanical injury of confluent cultured human EC by application of a 6 mm diameter cellulose polyacetate paper. Time for 50 % regeneration (T50) of the lesion was calculated after measuring the remaining lesion at time intervals. Human aFGF (brain) and bFGF (placenta) were purified by HPLC and identified by N-terminus analysis. They were used at concentrations that did not modify T50 when added to 5 % serum. HEP, LMWH and PPS (100 μg/ml) alone increased T50. Addition of HEP, LMWH, or PPS to aFGF markedly decreased T50. This effect was not present with bFGF, although their inhibitory effect alone was abolished. The FGFs alone or in the presence of HEP produce an increase in EC density. In this model, the repair of the EC lesion involves cell migration and proliferation and responds to the combined action of FGFs and HEP, LMWH or PPS. Thus, these drugs could be used to stimulate the repair of injured EC and prevent blood-vessel wall interactions leading to thrombosis or atherosclerosis.

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Al-Ansari, Dana E., Nura A. Mohamed, Isra Marei, Huseyin Yalcin und Haissam Abou-Saleh. „Assessment of Metal Organic Framework as Potential Drug Carriers in Cardiovascular Diseases“. In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0127.

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Background: Cardiovascular diseases (CVDs) are considered the major cause of death worldwide. Therapeutic delivery to the cardiovascular system may play an important role in the successful treatment of a variety of CVDs, including atherosclerosis, ischemic-reperfusion injury, and microvascular diseases. Despite their clinical benefits, current therapeutic drugs are hindered by their short half-life and systemic side effects. This limitation could be overcome using controlled drug release with the potential for targeted drug delivery using a nanomedicine approach. In the current study, we have assessed the use of a highly porous nano-sized preparation of iron-based Metal-organic Framework (MOF) commonly referred to as MIL-89 as potential drug carriers in the cardiovascular system. Aims: To assess the effect of MOFs on the viability and cytotoxicity of human vascular cells and the cellular uptake in vitro, and the organ-system toxicity of MOF in vivo using the Zebrafish model. Methods: Human pulmonary endothelial cells (HPAECs) and pulmonary smooth muscle cells (HPASMCs) were treated with variable concentrations of MOFs. The viability, cytotoxicity and anti-inflammatory effects were measured using AlamarBlue, LDH assay and ELISA. The cellular uptake of MOFs were assessed using light, confocal, and transmission electron microscopes and EDS analysis. Moreover, Zebrafish embryos were cultured and treated with MOFs-nanoparticles at 0 hours post fertilization (hpf) followed by different organ-specific assays at 24, 48, and 72 hpf. Results: Although MOFs affect the viability at high concentrations, it does not cause any significant cytotoxicity on HPAECs and HPASMCs. Interestingly, MOFs were shown to have an anti-inflammatory effect. Microscopic images showed an increased (concentration-dependent) cellular uptake of MOFs and transfer to daughter cells in both cell types. Moreover, the in vivo study showed that high concentrations of MOFs delay zebrafish embryos hatching and cause heart deformation, which is currently investigated using cardiotoxicity markers. Conclusion: MOFs is a promising nanoparticle prototypes for drug delivery in the cardiovascular system with high cellular uptake and anti-inflammatory effects. Further investigations of MOFs, including diseased models and drug- loaded formulation is required.

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O’Connell, Barry M., Tim M. McGloughlin und Michael T. Walsh. „Experimental Validation of the Influence of Stent Strut Compression on Artery Wall Drug Mass Transport“. In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206622.

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Atherosclerosis is a degenerative disease that affects coronary, carotid and other peripheral arteries in the body. Arterial occlusions ensuing from aggressive atherosclerotic plaque progression can often culminate in an ischemic attack, such as an apoplectic attack or a myocardial infarction [1–3]. Several interventional procedures are available to the clinician but in recent years drug eluting stents (DES) have become the preferred choice and by the beginning of 2006 more than 8 out of 10 coronary stents were DES [4] at a cost of between $4 and $5 billion annually [5].

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Bozsak, Franz, Jean-Marc Chomaz, Fulvio Martinelli und Abdul I. Barakat. „Modeling Arterial Wall Transport for Drug-Eluting Stents“. In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53871.

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Drug-eluting stents (DES) are very commonly used for treating coronary atherosclerotic lesions. Despite the broad effectiveness of DES, ∼5% of treated patients experience complications including in-stent restenosis and late-stent thrombosis. The occurrence of these complications depends on various factors including the concentration of the eluted drug in the arterial wall and the rate of arterial re-endothelialization. Drug concentration in the arterial wall needs to be sufficiently high to be efficacious while remaining sufficiently low to avoid compromising wall stability (leading to stent malapposition). Furthermore, because drugs used in DES modulate proliferation rates of not only smooth muscle cells but also endothelial cells, the drug concentration affects re-endothelialization rates. Drug concentration in the arterial wall is determined by the transport and metabolism of the drug and may also be affected by the flow field in the lumen of the stented vessel. In the present study, we develop a computational model of drug transport in the arterial wall. Previous models have typically treated the arterial wall as a homogeneous porous medium [1] and have often ignored drug reaction with cells in the arterial wall [2]. In the present study, we have developed a model that incorporates the multi-layer structure of the arterial wall and have compared its predictions for the distribution of an eluted drug within the arterial wall with those of the single-layer homogeneous wall model.

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Applegate, Brian E. „Simultaneous Morphological and Biochemical Imaging for Cancer Diagnosis and Atherosclerotic Plaque Discrimination“. In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/omp.2011.oma2.

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Yu, Miao, Vladimir Muzykantov und Alisa Morss Clyne. „Iron Oxide Nanoparticles Are Less Toxic to Endothelial Cells When Coated With Dextran and Polyethylene Glycol“. In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53702.

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Iron oxide nanoparticles are of particular interest for drug delivery applications, since they can be targeted to a specific location using a magnetic field. We are interested in delivering drugs to atherosclerotic plaques via these nanoparticles. However, prior to using nanoparticles in vivo, they must be shown as relatively non-toxic to cells. We and others have shown that bare iron oxide nanoparticles are readily taken up by cells, where they catalyze production of highly toxic reactive oxygen species [1]. This oxidative stress disrupts the cell cytoskeleton, alters cell mechanics, and may change other critical cell functions. Iron oxide nanoparticles for in vivo biomedical applications are often coated with a polysaccharide (eg. dextran) or a polymer (eg. polyethylene glycol, PEG). Both the size and the surface coating of the nanoparticle play an important role in cell toxicity.

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