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Colon submucous fibrovascular hamartoma: In a situation document.
Atherosclerosis, which is the most common chronic disease of the coronary artery, constitutes a vascular pathology induced by inflammation and plaque accumulation within arterial vessel walls. Both DNA methylation and histone modifications are epigenetic changes relevant for atherosclerosis. Recent studies have shown that the DNA methylation and histone modification systems are closely interrelated and mechanically dependent on each other. Herein, we explore the functional linkage between these systems, with a particular emphasis on several recent findings suggesting that histone acetylation can help in targeting DNA methylation and that DNA methylation may control gene expression during atherosclerosis.Dyslipidemia refers to an abnormal amount of lipid in the blood, and the total cholesterol level is defined as the sum of high-density lipoprotein cholesterol, low-density lipoprotein (LDL) cholesterol, and very-LDL cholesterol concentrations. In Korea, the westernization of lifestyle habits in recent years has caused an increase in the incidence of dyslipidemia, which is an important risk factor of cardiovascular disease (CVD). Several studies have been conducted on how dyslipidemia affects not only CVD, but also chorioretinal diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Recently, a pathological model of AMD was proposed under the assumption that AMD proceeds through a mechanism similar to that of atherosclerotic CVD. However, controversy remains regarding the relationship between chorioretinal diseases and lipid levels in the blood, and the effects of lipid-lowering agents. Herein, we summarize the role of lipids in chorioretinal diseases. In addition, the effects of lipid-lowering agents on the prevention and progression of chorioretinal diseases are presented.Ceramide and sphingomyelin (SM) are major components of the double membrane-bound sphingolipids. Ceramide is an essential bioactive lipid involved in numerous cell processes including apoptosis, necrosis, and autophagy-dependent cell death. Inversely, SM regulates opposite cellular processes such as proliferation and migration by changing receptor-mediated signal transduction in the lipid microdomain. SM is generated through a transfer of phosphocholine from phosphatidylcholine to ceramide by SM synthases (SMSs). Research during the past several decades has revealed that the ceramide/SM balance in cellular membranes regulated by SMSs is important to decide the cell fate, survival, and proliferation. In addition, recent experimental studies utilizing SMS knockout mice and murine disease models provide evidence that SMS-regulated ceramide/SM balance is involved in human diseases. Here, we review the basic structural and functional characteristics of SMSs and focus on their cellular functions through the regulation of ceramide/SM balance in membrane microdomains. In addition, we present the pathological or physiological implications of SMSs by analyzing their role in SMS-knockout mice and human disease models. This review finally presents evidence indicating that the regulation of ceramide/SM balance through SMS could be a therapeutic target for human disorders.Statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor) are among the most important medications for treating patients with acute myocardial infarction (AMI). Herein, we review the clinical benefit and future scope of statin therapy in Korean patients with AMI from the experience of the Korea AMI Registry. Statins are effective and safe in AMI patients, even in those with very low low-density lipoprotein cholesterol (LDL-C). Peri-procedural statin treatment could reduce the incidence of early stent thrombosis in patients with AMI after percutaneous coronary intervention. Reduction of high sensitivity C-reactive protein levels in patients with AMI plays an important role in the beneficial effect of statins on regression and compositional change of coronary plaques. Obtaining ≥50% reduction in LDL-C is associated with better clinical outcomes after AMI, whereas achieving less then 70 mg/dL LDL-C is not. Statin therapy has positive effects on clinical outcomes in patients with cardiogenic shock, ischemic heart failure, chronic kidney disease, and vasospasm. The combination of high-dose statin plus N-acetyl cysteine is associated with lower incidence of contrast-induced nephropathy in patients who underwent primary percutaneous coronary intervention. Moderate-intensity pitavastatin therapy is associated with a lower incidence of new-onset diabetes mellitus in patients with AMI and has similar clinical outcomes to moderate-intensity atorvastatin and rosuvastatin therapy. Future studies are required to assess the optimal intensity and LDL-C target concerning statin therapy, and the implementation of guidelines based cholesterol lowering practice in Korean patients with AMI.Atherosclerosis is the leading cause of life-threatening morbidity and mortality, as the rupture of atherosclerotic plaques leads to critical atherothrombotic events such as myocardial infarction and ischemic stroke, which are the 2 most common causes of death worldwide. Vascular calcification is a complicated pathological process involved in atherosclerosis, and microcalcifications are presumed to increase the likelihood of plaque rupture. Despite many efforts to develop novel non-invasive diagnostic modalities, diagnostic techniques are still limited, especially before symptomatic presentation. Navarixin cell line From this point of view, vulnerable plaques are a direct target of atherosclerosis imaging. Anatomic imaging modalities have the limitation of only visualizing macroscopic structural changes, which occurs in later stages of disease, while molecular imaging modalities are able to detect microscopic processes and microcalcifications, which occur early in the disease process. Na[18F]-fluoride positron emission tomography/computed tomography could allow the early detection of plaque instability, which is deemed to be a primary goal in the prevention of cardiac or brain ischemic events, by quantifying the microcalcifications within vulnerable plaques and evaluating the atherosclerotic disease burden.
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