Search results for "Lip"

The role of statins in preventing the progression of congestive heart failure in patients with metabolic syndrome.

2008

Heart Failure (CHF) is a very important public health problem in the world and certainly one of the most common debilitating diseases and cause of mortality. Current knowledge underlines that incidence rates are also influenced by the coexisting pathologic conditions that accelerate the development of disease or increase its severity. Important scientific evidence is emerging to demonstrate a strong correlation between HF and the metabolic syndrome (MetS). Hypolipemia- inducing medication offers the opportunity to discuss the possible existence of pharmacological substances that in addition to their specific targets have several demonstrated pleiotropic effects that could be beneficial in H…

A human hepatocellular in vitro model to investigate steatosis

2006

The present study was designed to define an experimental model of hepatocellular steatosis with a fat overaccumulation profile in which the metabolic and cytotoxic/apoptotic effects could be separated. This was accomplished by defining the experimental conditions of lipid exposure that lead to significant intracellular fat accumulation in the absence of overt cytotoxicity, therefore allowing to differentiate between cytotoxic and apoptotic effects. Palmitic (C16:0) and oleic (Cl 8: 1) acids are the most abundant fatty acids (FFAs) in liver triglycerides in both normal subjects and patients with nonalcoholic fatty liver disease (NAFLD). Therefore, human hepatocytes and HepG2 cells were incub…

Prostanoid release of cultured liver sinusoidal endothelial cells in response to endotoxin and tumor necrosis factor

1990

Abstract Vascular endothelial cells release prostanoids, especially prostacyclin, when properly stimulated. In addition to short acting stimuli like thrombin and histamine an increased prostanoid release occurs in the presence of endotoxin, interleukin 1 or tumor necrosis factor (TNF). The response of sinusoidal endothelial liver cells to such stimuli — probably important in hepatic inflammatory disease — is unknown. Sinusoidal endothelial liver cells from the guinea pig were isolated by centrifugal elutriation and investigated as confluent monolayers. Their prostanoid release in response to endotoxin and human recombinant TNF was determined by radioimmunoassays and compared to that obtaine…

P0760 : PNPLA3 rs738409 I748M is associated with steatohepatitis in non obese subjects with hepatitis C

2015

Complement C6 deficiency protects against diet-induced atherosclerosis in rabbits.

1998

Abstract —Low-density lipoprotein (LDL) can be transformed to an atherogenic moiety by nonoxidative, enzymatic degradation. Enzymatically degraded LDL induces macrophage foam cell formation, provokes release of cytokines, and also activates complement. To determine whether complement activation may contribute to atherogenesis, 6 pairs of homozygous C6-deficient rabbits and their non–C6-deficient heterozygous siblings were fed a cholesterol-rich diet for 14 weeks. Cholesterol levels and plasma lipoprotein profiles of the animals in the C6-competent and C6-deficient groups did not significantly differ, and the high density lipoprotein and LDL cholesterol ratios at the end of the experiment w…

Identification of a novel mutation of MTP gene in a patient with abetalipoproteinemia.

2011

Abetalipoproteinemia (ABL), or Bassen-Kornzweig syndrome, is a rare autosomal recessive disorder of lipoprotein metabolism, characterized by fat malabsorption, hypocholesterolemia retinitis pigmentosa, progressive neuropathy and acanthocytosis from early infancy. We describe the clinical and molecular characterization of a 6-month-old infant born of consanguineous, apparently healthy parents from Iran. The patient was hospitalized because of failure to thrive, greasy stool and vomiting. The patient's serum lipid profile, the clinical phenotype and the duodenal histology suggested the clinical diagnosis of ABL. The MTP gene analysis by direct sequencing revealed a novel homozygous mutation (…

Giant Nevus Lipomatosus Cutaneous Superficialis

2019

The effect of oral hormone replacement therapy on lipoprotein profile, resistance of LDL to oxidation and LDL particle size

2001

Abstract Objectives: To disclose if oral estradiol (E 2 ), alone or in combination with natural progesterone (P) or medroxyprogesterone acetate (MPA), may modify the oxidizability of low density lipoprotein (LDL), and if the effect is achieved at physiological dosages. LDL oxidizability was assessed by the resistance to oxidation by copper and by the particle size profile, since small particles have increased oxidation susceptibility. Methods: Thirty-three women received two consecutive, two-month length doses of 1 and 2 mg/day of oral E 2 . They were then randomly assigned to a fourteen-day treatment of 2 mg/day E 2 plus either 300 mg/day P or 5 mg/day MPA. A parallel group of experiments …

Selenoprotein synthesis and side-effects of statins.

2004

Statins are possibly the most effective drugs for the prevention and treatment of hypercholesterolaemia and coronary heart disease. They are generally well tolerated, however, they do cause some unusual side-effects with potentially severe consequences, most prominently myopathy or rhabdomyolysis and polyneuropathy. We noted that the pattern of side-effects associated with statins resembles the pathology of selenium deficiency, and postulated that the mechanism lay in a well established, but often overlooked, biochemical pathway--the isopentenylation of selenocysteine-tRNA([Ser]Sec). A negative effect of statins on selenoprotein synthesis does seem to explain many of the enigmatic effects a…

Acute methionine load‐induced hyperhomocysteinemia enhances platelet aggregation, thromboxane biosynthesis, and macrophage‐derived tissue factor acti…

1997

A moderate elevation of plasma homocysteine is a risk factor for atherosclerosis and arterial and veinous thrombosis. However, the mechanisms leading to vascular disorders are poorly understood because studies that have investigated the potential atherothrombogenicity of hyperhomocysteinemia in vivo are scarce. Using a rat model, we were the first to show that dietary folic acid deficiency, a major cause of basal hyperhomocysteinemia, is associated with enhanced macrophage-derived tissue factor and platelet activities. We proposed that an homocysteine-induced oxidative stress may account for this hypercoagulable state. To determine the true thrombogenicity of moderate hyperhomocysteinemia a…