Intake of dairy fat has long been considered as a risk factor for CVD. Pasture and dietary lipid supplementation have been reported to be reliable strategies in ruminant nutrition, in order to increase the content of a-linolenic acid (ALA), conjugated linoleic acid (CLA) and vaccenic acid (VA), and decrease SFA in milk fat. In the present study, we aimed at verifying whether consumption of a sheep cheese, naturally enriched in ALA, CLA and VA, would modify the plasma lipid and endocannabinoid profiles in mildly hypercholesterolaemic subjects. A total of forty-two adult volunteers (nineteen males and twenty-three females) with diagnosed mildly hypercholesterolaemia (total cholesterol 5·68 -7·49 mmol/l) were randomly assigned to eat 90 g/d of a control or enriched cheese for 3 weeks, with a cross-over after 3 weeks of washout. Plasma lipids, endocannabinoids, adipokines and inflammatory markers were measured. The intake of enriched cheese significantly increased the plasma concentrations of CLA, VA, the n-3 fatty acids ALA and EPA, and more remarkably decreased that of the endocannabinoid anandamide. LDL-cholesterol decreased significantly (7 %). No changes were detected in the levels of inflammatory markers; however, a significant correlation was found between the plasma levels of anandamide and leptin. The control cheese modified none of the parameters measured. The results obtained do not support the view that intake of dairy fat is detrimental to hypercholesterolaemic subjects. Indeed, they show that a naturally enriched cheese possesses beneficial properties, since it ameliorates the plasma lipid profile, and more remarkably reduces endocannabinoid biosynthesis.
Tumour are characterised by a high content of cholesteryl esters (CEs) stored in lipid droplets purported to be due to a high rate of intracellular esterification of cholesterol. To verify whether and which pathways involved in CE accumulation are essential in tumour proliferation, the effect of CE deprivation, from both exogenous and endogenous sources, on CEM-CCRF cells was investigated. Cholesterol synthesis, esterification and content, low-density lipoprotein (LDL) binding and high-density lipoprotein (HDL)-CE uptake were evaluated in cultured in both conventional and delipidated bovine serum with or without oleic or linoleic acids, cholesteryl oleate, LDL and HDL. High content of CEs in lipid droplets in this cell line was due to esterification of both newly synthesised cholesterol and that obtained from hydrolysis of LDL; moreover, a significant amount of CE was derived from HDL-CE uptake. Cell proliferation was slightly affected by either acute or chronic treatment up to 400 μM with Sz-58035, an acyl-cholesteryl cholesterol esterification inhibitor (ACAT); although when the enzyme activity was continuously inhibited, CE content in lipid droplets was significantly higher than those in control cells. In these cells, analysis of intracellular and medium CEs revealed a profile reflecting the characteristics of bovine serum, suggesting a plasma origin of CE molecules. Cell proliferation arrest in delipidated medium was almost completely prevented in the first 72 h by LDL or HDL, although in subsequent cultures with LDL, it manifested an increasing mortality rate. This study suggests that high content of CEs in CEM-CCRF is mainly derived from plasma lipoproteins and that part of CEs stored in lipid droplets are obtained after being taken up from HDL. This route appears to be up-regulated according to cell requirements and involved in low levels of c-HDL during cancer. Moreover, the dependence of tumour cells on a source of lipoprotein provides a novel impetus in developing therapeutic strategies for use in the treatment of some tumours.
Osteoarticular infections, although uncommon, represent a severe condition in neonates. Infections in newborns are largely of an acute nature, transmitted by hematogenous means. The most frequently observed etiological agents are: Staphylococcus aureus, Gram negative and group B Streptococcus spp. In the majority of cases the metaphyses of the long bone are the most commonly implicated sites, although infection may spread to the contiguous epiphysis and joint in neonates. Diagnosis of acute septic arthritis and osteomyelitis may be hindered, especially in neonates, due to the manifestation of less clear-cut characteristic symptoms and signs compared to in children. When osteomyelitis is suspected, imaging techniques used in association with blood and tissue cultures are the most reliable diagnostic tests. Antimicrobial treatment should be administered for 3-4 weeks, initially intravenously, later switching to oral medication. Surgery is indicated to drain acute abscesses or when no improvement is achieved following antibiotic treatment.
This article is available online at http://www.jlr.org hallmark of atherosclerosis. Similar changes are present in chronic metabolic diseases (hypercholesterolemia, insulin resistance, diabetes, etc.) ( 4 ), and have been described in other disorders such as cancer ( 5-9 ) and infections ( 10 ). Probably, accumulation of CEs serves as a reservoir of cholesterol for an enhanced membrane biogenesis during sustained proliferation.During acute infections the body undergoes several metabolic changes ( 11,12 ), among which plasma lipid alterations are prominent and related to a shift in energetic requirements (increased triglycerides and fatty acids) ( 13,14 ) or to structural modifi cation of LDLs ( 15 ) and HDLs ( 16,17 ). The infection-related decrease in C-HDLs observed in all species is ascribed to a reduction of proteins involved in reverse cholesterol transport ( 18,19 ), supposedly induced by infl ammatory molecules secreted from immune cells activated by the microbial stimulus ( 16 ). Thus, during infection, an ineffi cient removal of cholesterol from the arteries may contribute toward eliciting a lipid overload of macrophages and transformation of the former into foam cells ( 19 ). For this reason, infections have been considered as a serious risk factor for the development or worsening of atherosclerosis (20)(21)(22). Epidemiological fi ndings support this correlation, with acute vascular accidents (myocardial infarction, ictus, etc.) being described during acute and chronic infections. Carotid plaques have been observed in patients with periodontal diseases ( 23, 24 ) and other chronic infections ( 25,26 ).
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