Ultrasound, anthropometry and bioimpedance: a comparison in predicting fat deposition in non-alcoholic fatty liver disease.

Purpose: The aim of our study was the evaluation of anthropometric measurements [waist circumference and sagittal abdominal diameter (SAD)] and abdominal bioelectrical impedance analysis (BIA) (ViScan, TANITA) in comparison to several abdominal ultrasonographic (US) measurements to estimate visceral fat deposition and liver steatosis in a population of 105 subjects.

Methods: All 105 patients underwent a complete anthropometric evaluation, blood sample for the determination of total cholesterol, HDL cholesterol, triglycerides, glucose, insulin, high-sensitivity C-reactive protein, BIA and US measurements (peritoneal, pre-peritoneal, peri-renal, para-renal and peri-hepatic fat thickness).

Results: All the ultrasonographic markers considered in our study are related to the presence of non-alcoholic fatty liver disease (NAFLD), and so is true for SAD.

LDL density and oxidation are modulated by PON1 promoter genotype in patients with Alzheimer's disease.

Cholesterol metabolism alteration is a hot topic in the field of Alzheimer's disease (AD). However, data on plasma lipoproteins cholesterol distribution and oxidation in AD and their possible genetic determinants are lacking. The paraoxonase-1 (PON1) gene -107C/T promoter polymorphisms have been found associated with AD.

Involvement of the tubular ClC-type exchanger ClC-5 in glomeruli of human proteinuric nephropathies.

Unlabelled: Glomerular protein handling mechanisms have received much attention in studies of nephrotic syndrome. Histopathological findings in renal biopsies from severely proteinuric patients support the likelihood of protein endocytosis by podocytes. ClC-5 is involved in the endocytosis of albumin in the proximal tubule.

Early activation of fibrogenesis in transplanted kidneys: a study on serial renal biopsies.

Background/aims: In kidney transplants, the renin-angiotensin system (RAS) is involved in systemic and local changes that may induce fibrosis. Our aim was to use gene expression and immunohistochemical analysis to investigate the RAS and several factors involved in the fibrogenic cascade in allograft biopsies.

Methods: We considered 43 donor biopsies (T0), 18 biopsies obtained for diagnostic purposes (Td) and 24 protocol biopsies (Tp) taken 2 months after transplantation in patients with stable renal function.

Small dense LDL and VLDL predict common carotid artery IMT and elicit an inflammatory response in peripheral blood mononuclear and endothelial cells.

Objective: The presence of small dense LDL has been associated with increased cardiovascular risk and with the progression of coronary and carotid atherosclerosis in case-control and prospective studies. The aim of this study was to investigate the relation between different lipoprotein subfractions with intima-media thickness of the common carotid artery in a free-living, healthy population, and to evaluate whether in patients with comparable LDL-C, the different lipoprotein subclasses differently affected the expression of chemokines, cytokines and adhesion molecules in peripheral blood mononuclear and endothelial cells.

Methods And Results: The lipoprotein cholesterol profile and the LDL buoyancy (LDL-RF) were evaluated in a cohort of 156 healthy subjects randomly selected from the PLIC (Progressione Lesione Intimale Carotidea) study.

Common hepatic lipase gene promoter variant predicts the degree of neointima formation after carotid endarterectomy: impact of plaque composition and lipoprotein phenotype.

Background: The common -514 C-T promoter polymorphism of the hepatic lipase gene (LIPC) and the cholesteryl ester transfer protein (CETP) gene TaqIB polymorphism affect atherogenesis. We investigated the potential relationship between these polymorphisms and the maximum-intima-media thickness (M-IMT) after carotid endarterectomy.

Methods: The LIPC and CETP genotypes were determined by PCR in 68 patients undergoing endarterectomy.

Heparin reduces glomerular infiltration and TGF-beta protein expression by macrophages in puromycin glomerulosclerosis.

Background: In a number of experimental models of nephropathy, heparin is renoprotective because it inhibits mesangial matrix synthesis and cell proliferation; in most of these models, glomerular macrophage infiltration has a pathogenic role. We investigated the hypothesis that heparin might also be renoprotective by modulating the macrophages in various ways in the chronic puromycin glomerulosclerosis model.

Methods: We studied the effect of a 3 month course, two different dosages of a non-anticoagulant heparin by immunohistochemical evaluation of the number of macrophages (ED-1 positive cells) in glomeruli, as well as the expression and deposition of TGF-beta and latent TGF-beta binding protein in foam cells and mesangial matrix.