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Fresh Study Tensile Physical Components along with Strengthening Percentage involving Steel-Plastic Substance Geogrid-Reinforced Belt.
Insight into the subcellular trafficking machinery of CD36 will provide novel targets to treat the lipid-overloaded heart. A screen for CD36-dedicated trafficking proteins found that vacuolar-type H+-ATPase and specific vesicle-associated membrane proteins, among others, were uniquely involved in CD36 recycling. Preliminary data suggest that these proteins may offer clues on how to manipulate myocardial lipid uptake, and thus could be promising targets for metabolic intervention therapy to treat the failing heart.Ceramides are minor components of the hepatic lipidome that have major effects on liver function. These products of lipid and protein metabolism accumulate when the energy needs of the hepatocyte have been met and its storage capacity is full, such that free fatty acids start to couple to the sphingoid backbone rather than the glycerol moiety that is the scaffold for glycerolipids (e.g., triglycerides) or the carnitine moiety that shunts them into mitochondria. As ceramides accrue, they initiate actions that protect cells from acute increases in detergent-like fatty acids; for example, they alter cellular substrate preference from glucose to lipids and they enhance triglyceride storage. When prolonged, these ceramide actions cause insulin resistance and hepatic steatosis, 2 of the underlying drivers of cardiometabolic diseases. selleck kinase inhibitor Herein the author discusses the mechanisms linking ceramides to the development of insulin resistance, hepatosteatosis and resultant cardiometabolic disorders.Cardiomyopathy is the leading cause of mortality worldwide. While the causes of cardiomyopathy continue to be elucidated, current evidence suggests that aberrant bioactive lipid signaling plays a crucial role as a component of cardiac pathophysiology. Sphingolipids have been implicated in the pathophysiology of cardiovascular disease, as they regulate numerous cellular processes that occur in primary and secondary cardiomyopathies. Experimental evidence gathered over the last few decades from both in vitro and in vivo model systems indicates that inhibitors of sphingolipid synthesis attenuate a variety of cardiomyopathic symptoms. In this review, we focus on various cardiomyopathies in which sphingolipids have been implicated and the potential therapeutic benefits that could be gained by targeting sphingolipid metabolism.Post-transcriptional regulations of mRNA transcripts such as alternative splicing and alternative polyadenylation can affect the expression of genes without changing the transcript levels. Recent studies have demonstrated that these post-transcriptional events can have significant physiological impacts on various biological systems and play important roles in the pathogenesis of a number of diseases, including cancers. Nevertheless, how cellular signaling pathways control these post-transcriptional processes in cells are not very well explored in the field yet. The mammalian target of rapamycin complex 1 (mTORC1) pathway plays a key role in sensing cellular nutrient and energy status and regulating the proliferation and growth of cells by controlling various anabolic and catabolic processes. Dysregulation of mTORC1 pathway can tip the metabolic balance of cells and is associated with a number of pathological conditions, including various types of cancers, diabetes, and cardiovascular diseases. Numerous reports have shown that mTORC1 controls its downstream pathways through translational and/or transcriptional regulation of the expression of key downstream effectors. And, recent studies have also shown that mTORC1 can control downstream pathways via post-transcriptional regulations. In this review, we will discuss the roles of post-transcriptional processes in gene expression regulations and how mTORC1-mediated post-transcriptional regulations contribute to cellular physiological changes. We highlight post-transcriptional regulation as an additional layer of gene expression control by mTORC1 to steer cellular biology. These emphasize the importance of studying post-transcriptional events in transcriptome datasets for gaining a fuller understanding of gene expression regulations in the biological systems of interest.The number of the elderly individuals is steeply increasing, and their absolute cardiovascular risk is higher than that of younger age groups. link2 However, very few statin trials have included elderly patients alone. Recently, we published the SCOPE-75 study, which analyzed the effect of statins for primary prevention in elderly Koreans (>75 years). In this study, statin users showed significantly fewer cardiovascular events and a lower all-cause mortality rate, supporting more active use of statins in this population. In the current review, we further compare and discuss similar studies reported in the past decades and in recent years.
The aim of this study was to investigate the effects of 2 anti-malarial drugs, chloroquine (CQ) and hydroxychloroquine (HCQ), on inhibition of vascular smooth muscle cell (VSMC) proliferation both
and
via Adenosine monophosphate-activated protein kinase (AMPK) activation.

Protein and mRNA levels were determined by western blot analysis and real-time reverse transcription-polymerase chain reaction in primary rat VSMCs treated with CQ and HCQ, respectively. Cell proliferation was measured by flow cytometry and cell counting. Mice carotid arteries were ligated and treated with CQ or HCQ every other day for 3 weeks. Pathological changes of carotid arteries were visualized by both microscopy and fluorescence microscopy.

CQ and HCQ increase AMPK phosphorylation in VSMCs. Both CQ and HCQ decrease platelet-derived growth factor-induced VSMC proliferation and cell cycle progression in an AMPK-dependent manner. In addition, CQ and HCQ inhibit Smad3 phosphorylation and VSMC proliferation induced by transforming growth factor-β1. Moreover, CQ and HCQ diminished neointimal proliferation in a mouse model of carotid artery ligation-induced neointima formation.

The results demonstrated that CQ and HCQ inhibit cell proliferation and cell cycle progression in VSMCs via the AMPK-dependent signaling pathway. Carotid artery ligation-induced intima thickness was reduced in mouse arteries treated with CQ or HCQ, suggesting a role for antimalarial drugs in treating atherosclerosis and restenosis.
The results demonstrated that CQ and HCQ inhibit cell proliferation and cell cycle progression in VSMCs via the AMPK-dependent signaling pathway. Carotid artery ligation-induced intima thickness was reduced in mouse arteries treated with CQ or HCQ, suggesting a role for antimalarial drugs in treating atherosclerosis and restenosis.
Fatty liver is associated with insulin resistance-related diseases, such as dyslipidemia, obesity, and type 2 diabetes. The aim of this study was to evaluate the association of dyslipidemia with fatty liver and assess the differences in these associations according to the degree of hepatic steatosis.

A total of 2,462 subjects (1,679 men and 783 women) who underwent a comprehensive health check-up (including abdominal computed tomography) from January 2010 to December 2013 were enrolled at Samsung Changwon Hospital Healthcare Center. The liver attenuation index (LAI), defined as the difference between mean hepatic and splenic attenuation, was used to assess the degree of hepatic steatosis. An LAI below 5 Hounsfield units was defined as fatty liver.

We found that 32.2% of the study subjects had fatty liver. Serum low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG), and fasting blood glucose concentrations and glycated hemoglobin (HbA1c percentage) were significant greater in the fatty liver group compared with the non-fatty liver group, while serum high-density lipoprotein cholesterol (HDL-C) was significantly lower in the fatty liver group. Subjects with fatty liver had 1.7-fold greater risk of dyslipidemia than those without fatty liver after adjusting for age, sex, body mass index (BMI), and HbA1c. When individuals with fatty liver were analyzed by tertiles of LAI values, LDL-C, TG, fasting glucose, BMI, and HbA1c concentrations increased while HDL-C decreased with decreasing LAI tertiles. Compared with LAI tertile 3, the risk for dyslipidemia significantly increased with adjusted odds ratios of 1.42, and 1.81 in tertiles 2 and 1, respectively.

Fatty liver was significantly associated with dyslipidemia and this association varied according to the degree of hepatic steatosis.
Fatty liver was significantly associated with dyslipidemia and this association varied according to the degree of hepatic steatosis.
The aim of this study was to examine the associations of cholesterol ester transfer protein (
) rs6499861 and rs12708980 with high-density lipoprotein cholesterol (HDL-C) considering obesity and family history of diabetes (FHD) in Korean men and women.

We analyzed the association of
single nucleotide polymorphisms (SNPs) with HDL-C among individuals selected from a hospital (n=4 294) and the Bundang-gu area in Korea (n=2 304).

We found that the
SNP rs6499861 was associated with a lower HDL-C level (effect per allele -2.044 mg/dL,
<0.0001). Individuals with a rs6499861 CG/GG genotype had a 1.45-fold higher risk of an abnormal level of HDL-C (<40 mg/dL) than those with a CC genotype. This genotype-HDL-C association was stronger in women (odds ratio [OR], 1.99; 95% confidence interval [CI], 1.39-2.85) compared with men (OR, 1.33; 95% CI, 1.10-1.61) and in women with a FHD (OR, 4.82; 95% CI, 1.86-12.5;
=0.0012) compared with women without a family history. Relative to individuals with a CC genotype and body mass index (BMI) <25.69 kg/m
, individuals with a CG/GG genotype and BMI ≥25.69 kg/m
had an OR (95% CI) of 2.61 (1.97-3.47).

These findings indicate that
variants are linked to HDL-C level in Koreans and that this link is stronger in obese men and in women who have a FHD.
These findings indicate that CETP variants are linked to HDL-C level in Koreans and that this link is stronger in obese men and in women who have a FHD.
The aim of this study was to evaluate under target rates of low-density lipoprotein-cholesterol (LDL-C) in Korean patients with stable coronary artery disease (CAD) or an acute coronary syndrome (ACS) in real world practice.

Dyslipidemia International Study II was an international observational study of patients with stable CAD or an ACS. Lipid profiles and use of lipid-lowering therapy (LLT) were documented at enrollment, and for the ACS cohort, 4 months follow-up was recommended. Rates of under target LDL-C as per European guidelines, were evaluated, and multivariate regression was performed to identify predictive factors of patients presenting under the target.

A total of 808 patients were enrolled in Korea, 500 with stable CAD and 308 with ACS. Of these, 90.6% and 52.6% were being treated with LLT, respectively. In the stable CAD group, 40.0% were under target LDL-C, while in ACS group, the rate was 23.7%. A higher statin dose was independently associated with under target LDL-C in both groups (OR, 1.03;
=0.046 [stable CAD] and OR, 1.05;
=0.01 [ACS]). link3 The mean statin dosage (atorvastatin equivalent) was 17 mg/day. In the 79 ACS patients who underwent the follow-up examination, the LDL-C under target rate rose to 59.5%.

Only a minority of patients with stable CAD or ACS were under their target LDL-C level at enrollment. The statin dose was not sufficient in the majority of patients. These results indicate a considerable LLT gap in Korean patients with established CAD.
Only a minority of patients with stable CAD or ACS were under their target LDL-C level at enrollment. The statin dose was not sufficient in the majority of patients. These results indicate a considerable LLT gap in Korean patients with established CAD.
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