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Realtek High Definition Audio drivers R2.7. - New version of High Definition Audio drivers for sound card from the company Realtek, drivers are designed for operating systems Windows 200X, Windows XP, Vista, Windows 7, Windows 8, Windows 8.1 - 32/64 bit.Info about the driver:Name: Realtek High Definition Audio drivers(High Definition Audio System Software - Realtek ALC Audio drivers)Package version driver: R2.72 (3.75)Win 200X, XP driver version: 188.8.131.5271Win Vista driver version: 184.108.40.20671Version drivers Win 7, Win 8/8.1: 220.127.116.1171Drivers Date: 22.10.2013OS: Windows 200X, Windows XP, Windows 7, Windows 8, Windows 8.1 - 64 bitsSupported chipsets:ALC1150, ALC663, ALC662, ALC665, ALC680, ALC260, ALC262, ALC882, ALC885, ALC883, ALC880, ALC888, ALC889, ALC861VC, ALC861VD, ALC892, ALC660,, ALC269, ALC268, ALC267, ALC273, ALC272, ALC270, ALC887, ALC670, ALC275.HDMI Device WHQL Support: ATI HDMI DevicesOS Supporting: Microsoft Windows XP, Windows 2000, Windows Server 2003, Vista, Windows Server 2008, Windows7, Windows 8, Windows 8.1 - x86/x64Pack with Microsoft High Definition Audio UAAV1.0a(5013) For Windows 2000 SP4, XP SP1, XP SP2, Server 2003 SP1.Add/Fix1) Driver:Customizations;Add Codec ALC255, ALC235, ALC867;Support Windows 8.1.
For many years, cardiovascular disease (CVD) has been the leading cause of death around the world. Often associated with CVD are comorbidities such as obesity, abnormal lipid profiles and insulin resistance. Insulin is a key hormone that functions as a regulator of cellular metabolism in many tissues in the human body. Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance is characterized by defects in uptake and oxidation of glucose, a decrease in glycogen synthesis, and, to a lesser extent, the ability to suppress lipid oxidation. Literature widely suggests that free fatty acids are the predominant substrate used in the adult myocardium for ATP production, however, the cardiac metabolic network is highly flexible and can use other substrates, such as glucose, lactate or amino acids. During insulin resistance, several metabolic alterations induce the development of cardiovascular disease. For instance, insulin resistance can induce an imbalance in glucose metabolism that generates chronic hyperglycemia, which in turn triggers oxidative stress and causes an inflammatory response that leads to cell damage. Insulin resistance can also alter systemic lipid metabolism which then leads to the development of dyslipidemia and the well-known lipid triad: (1) high levels of plasma triglycerides, (2) low levels of high-density lipoprotein, and (3) the appearance of small dense low-density lipoproteins. This triad, along with endothelial dysfunction, which can also be induced by aberrant insulin signaling, contribute to atherosclerotic plaque formation. Regarding the systemic consequences associated with insulin resistance and the metabolic cardiac alterations, it can be concluded that insulin resistance in the myocardium generates damage by at least three different mechanisms: (1) signal transduction alteration, (2) impaired regulation of substrate metabolism, and (3) altered delivery of substrates to the myocardium. The aim of this review is to discuss the mechanisms associated with insulin resistance and the development of CVD. New therapies focused on decreasing insulin resistance may contribute to a decrease in both CVD and atherosclerotic plaque generation.
Insulin is a potent anabolic hormone that exerts a variety of effects on many types of cells. Some of the main metabolic actions of insulin are stimulating glucose uptake in skeletal muscles and adipocytes, promoting glycogen synthesis in skeletal muscles, suppressing hepatic glucose production, and inhibiting lipolysis in adipocytes . After ingestion, insulin is secreted from the pancreas and induces the uptake of circulating glucose in its target tissues by binding to an insulin receptor. This binding activates receptor autophosphorylation, which triggers a downstream signaling cascade through the phosphorylation of tyrosine residues of the insulin receptor substrates, IRS (IRS-1 or IRS-2), followed by phosphorylation of phosphatidylinositol 3-kinase (PI3K), phosphoinositide dependent kinase-1, Akt (Akt1 and Akt2), protein kinase C (PKC) and mammalian target of rapamycin (mTOR), as well as ribosomal protein S6 kinase beta 1 (S6K1) [10, 11]. These events result in an increased translocation of the glucose transporter 4 (GLUT4) to the membrane, thus facilitating glucose uptake . After uptake, free glucose is rapidly phosphorylated to glucose 6-phosphate (G6P), which subsequently enters different metabolic pathways .
A simplified model of insulin resistance. The loss of suppressive effects of insulin on lipolysis in adipocytes increases free fatty acids. Increased free fatty acids flux to the liver stimulates the assembly and secretion of VLDL resulting in hypertriglyceridemia. Triglycerides (TG) in VLDL are transferred to both HDL and LDL through the action of cholesteryl ester transfer protein (CETP). This process results in a triglyceride-enriched HDL and LDL particle. Triglyceride-enriched HDL is more rapidly cleared from the circulation by the kidney, leaving fewer HDL particles to accept cholesterol from the vasculature. In the glucose metabolism, the insulin resistance results in decreased hepatic glycogen synthesis, owing to decreased activation of glycogen synthase, increased hepatic gluconeogenesis, and glucose delivery by the liver
In relation to external factors, the increase in free fatty acids (FFA) induced by obesity can trigger insulin resistance through lipid accumulation (ectopic lipids). This may activate atypical PKC that inhibits insulin signaling and insulin-stimulated glucose uptake in skeletal muscles, as well as decreases the insulin-stimulated hepatic glycogen synthesis [43, 44]. This can lead to insulin resistance and increased glucose delivery by the liver . Additionally, FFA triggers insulin resistance by direct activation of Toll-like Receptor 4 (TLR4) and the innate immune response .
Obesity is a world-wide epidemic and intimately associated with the development of type 2 diabetes and CVDs. Visceral and epicardial adiposity related to obesity are the major drivers for cardiac disease in these individuals . Obesity has a major effect in modifying the lipoprotein profile and factors associated with systemic and vascular inflammation, and endothelial dysfunction . Abnormal concentrations of lipids and apolipoproteins can produce changes in the production, conversion, or catabolism of lipoprotein particles. These changes may contribute to increased basal lipolysis in obesity and the release of fatty acids into the circulation that consequences a proatherogenic phenotype [19, 90].
Glucose uptake is mediated via glucose transporters. There are two different types of transporters, the Na2+-coupled carrier system and the facilitative glucose transporters (GLUT). GLUT1 and GLUT4 are the major players for glucose transport in the heart. GLUT4 represents the major mechanism that regulates glucose entry in the beating heart, with GLUT1 playing a lesser role as it is primarily localized on plasma membranes and is responsible for basal cardiac glucose uptake. GLUT4 is mostly present in the intracellular vesicles at resting stages and is translocated to the plasma membrane upon insulin stimulation . After uptake, free glucose is rapidly phosphorylated to glucose 6-phosphate (G6P), which subsequently enters many metabolic pathways . Glycolysis represents the major pathway in glucose and yields pyruvate for subsequent oxidation. Beside glycolysis, G6P also may be channeled into glycogen synthesis or the pentose phosphate pathway (PPP). The PPP is an important source of NADPH, which plays a critical role in regulating cellular oxidative stress and is required for lipid synthesis .
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