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{userid:"alessandro.uzzau", "refid":140,"attachment":"","articletype":"article","sectionheading":"","title":"Su alcuni aspetti di fisiopatologia digestiva dopo interventi di gastrectomia totale","year":"1989","author":"F Bresadola, P Soro, L Noce, P Muretti, B Perrone, A Uzzau, A Pacifico, L Falchi, G Meloni, F Melis, GM Arca","journal":"Acta Chirurgica Italica","volume":"45","number":"1","pages":"175-180","month":"","doi":"","pubmed":"","pdflink":"","urllink":"","abstract":"","note":"","tags":""}
,

{userid:"alberto.signore", "articletype":"article","pages":"802-809","author":"G Zuliani, M Arca, A Signore, G Bader, S Fazio, M Chianelli, S Bellosta, F Campagna, A Montali, M Maioli, A Pacifico, G Ricci, R Fellin","year":"1999","title":"Characterization of a new form of inherited hypercholesterolemia: familial recessive hypercholesterolemia.","month":"Mar","journal":"Arterioscler Thromb Vasc Biol","publisher":"","volume":"19","number":"3","note":"","tags":"Adult,Apolipoprotein B-100,Apolipoproteins B,Cholesterol, LDL,Family Health,Female,Genes, Recessive,Humans,Hypercholesterolemia,Italy,Kidney,Kinetics,Liver,Male,Middle Aged,Myocardium,Pedigree,Receptors, LDL,Spleen","booktitle":"","editor":"","abstract":"We previously described a Sardinian family in which the probands had a severe form of hypercholesterolemia, suggestive of familial hypercholesterolemia (FH). However, low density lipoprotein (LDL) receptor activity in fibroblasts from these subjects and LDL binding ability were normal. The characteristics of the pedigree were consistent with an autosomal recessive trait. Sitosterolemia and pseudohomozygous hyperlipidemia were ruled out. A second Sardinian kindred with similar characteristics was identified. Probands showed severe hypercholesterolemia, whereas their parents and grandparents were normolipidemic. FH, familial defective apoprotein (apo) B, sitosterolemia, and cholesteryl ester storage disease were excluded by in vitro studies. We addressed the metabolic basis of this inherited disorder by studying the in vivo metabolism of LDL in 3 probands from these 2 families. 125I-LDL turnover studies disclosed a marked reduction in the fractional catabolic rate (0.19+\/-0.01 versus 0.36+\/-0.03 pools per day, respectively; P<0.001) and a significant increase in the production rate [20.7+\/-4.4 versus 14. 0+\/-2.4 mg. kg-1. d-1, respectively; P<0.01] of LDL apoB in the probands compared with normolipidemic controls. We then studied the in vivo biodistribution and tissue uptake of 99mtechnetium-labeled LDL in the probands and compared them with those in normal controls and 1 FH homozygote. The probands showed a significant reduction in hepatic LDL uptake, similar to that observed in the FH homozygote. A reduced uptake of LDL by the kidney and spleen was also observed in all patients. Our findings suggest that this recessive form of hypercholesterolemia is due to a marked reduction of in vivo LDL catabolism. This appears to be caused by a selective reduction in hepatic LDL uptake. We propose that in this new lipid disorder, a recessive defect causes a selective impairment of LDL receptor function in the liver.","address":"","school":"","issn":"1079-5642","doi":"","pubmed":"10073989","key":"Zuliani1999","howpublished":"","urllink":"","refid":64}
,

{userid:"alberto.signore", "articletype":"article","pages":"117-126","author":"Alessio Annovazzi, Elena Bonanno, Marcello Arca, Calogero D'Alessandria, Antonella Marcoccia, Luigi G Spagnoli, Francesco Violi, Francesco Scopinaro, Giorgio De Toma, Alberto Signore","year":"2006","title":"99mTc-interleukin-2 scintigraphy for the in vivo imaging of vulnerable atherosclerotic plaques.","month":"Feb","journal":"Eur J Nucl Med Mol Imaging","publisher":"","volume":"33","number":"2","note":"","tags":"Aged,Aged, 80 and over,Anticholesteremic Agents,Atherosclerosis,Carotid Arteries,Diet, Atherogenic,Female,Heptanoic Acids,Humans,Hydroxymethylglutaryl-CoA Reductase Inhibitors,Inflammation,Interleukin-2,Male,Middle Aged,Pyrroles,Radionuclide Imaging,Technetium","booktitle":"","editor":"","abstract":"PURPOSE: Several histopathological studies have demonstrated that vulnerable plaques are enriched in inflammatory cells. The aims of this study were: (1a) to test the ability of 99mTc-labelled interleukin-2 (99mTc-IL2) to bind to IL2R-positive (IL2R+) cells in carotid plaques and (1b) to correlate the plaque uptake of 99mTc-IL2, measured in vivo, with the number of IL2R+ cells within the plaque, measured ex vivo by histology (transversal study, TS), and (2) to evaluate changes in 99mTc-IL2 uptake in plaques, before and after treatment with a statin or a hypocholesterolaemic diet (longitudinal study, LS). METHODS: Ultrasound scan was performed for plaque characterisation and localisation. Fourteen patients (16 plaques) eligible for endoarterectomy were recruited for the TS and underwent 99mTc-IL2 scintigraphy before surgery. Nine patients (13 plaques) were recruited for the LS; these patients received atorvastatin or a standard hypocholesterolaemic diet and 99mTc-IL2 scintigraphy was performed before and after 3 months of treatment. RESULTS: The degree of 99mTc-IL2 uptake was expressed as the plaque\/background (T\/B) ratio. In patients from TS, T\/B ratios correlated with the percentage of IL2R+ cells at histology (r = 0.707; p = 0.002) and the number of IL2R+ cells at flow cytometry (r = 0.711; p = 0.006). No correlations were observed between ultrasound scores and either scintigraphic or histological findings. In patients from the LS, the mean 99mTc-IL2 uptake decreased in statin-treated patients (1.75+\/-0.50 vs 2.16+\/-0.44; p = 0.012), while it was unchanged in the patients on the hypocholesterolaemic diet (2.33+\/-0.45 vs 2.34+\/-0.5). CONCLUSION: 99mTc-IL2 accumulates in vulnerable carotid plaques; this accumulation is correlated with the amount of IL2R+ cells and is influenced by lipid-lowering treatment with a statin.","address":"","school":"","issn":"1619-7070","doi":"10.1007\/s00259-005-1899-4","pubmed":"16220305","key":"Annovazzi2006","howpublished":"","urllink":"","refid":21}
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{userid:"lucio.sibilia", "refid":"22","attachment":"","articletype":"article","sectionheading":"","title":"Association of Serum Selenium with Selected Cardiovascular Risk Factors  , Vol. 51 Issue: Numbers 1-2 p170-180.","year":"1995","author":"Menditto, A.; Chiodo, F.; Giampaoli, S.; Menotti, A.; Ricci, G.; Urbinati, G.C.; Angelico, F.; Arca, M.; Bucci, A.; Buongiorno, A.M.; Consalvi, D.; Conti, R.; Dangelo, G.; Defilippis, A.; Delben, M.; Delmonaco, E.; Fazio, S.; Montali, A.; Pannozzo, F.; Pontecorvi, A.; Ricci, P.; Sibilia, L.; Sotis, G.L.; Stefanutti, C.; Volpe, R.; Barzotti, S.; Capelli, M.; Capocaccia, R.; Dicarlo, G.; Dima, F.; Lonoce, C.; Lombari, P.; Pasquali, M.; Santaquilani, A.; Verdecchia, A.; Morisi, G.","journal":"Microchemical Journal","volume":"51","number":"1-2","pages":"170-180","month":"","doi":"","pubmed":"","pdflink":"","urllink":"","abstract":"","note":"","tags":""}
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