نتایج جستجو برای: familial defective apolipoprotein

تعداد نتایج: 117246  

Journal: :Arteriosclerosis and thrombosis : a journal of vascular biology 1991
N B Myant J J Gallagher B L Knight S N McCarthy J Frostegård J Nilsson A Hamsten P Talmud S E Humphries

In a previous study (Tybjaerg-Hansen et al, Atherosclerosis 1990;80:235-242), we identified nine patients heterozygous for the apolipoprotein B (apo B) arginine-to-glutamine (Arg3,500----Gln) mutation (familial defective apolipoprotein B-100 [FDB]). Six of these had been diagnosed clinically as familial hypercholesterolemic (FH) heterozygotes. We have since examined low density lipoprotein (LDL...

2000
S. Bertolini A. Cantafora M. Averna C. Cortese C. Motti S. Martini G. Pes A. Postiglione C. Stefanutti I. Blotta L. Pisciotta S. Calandra

Seventy-one mutations of the low density lipoprotein (LDL) receptor gene were identified in 282 unrelated Italian familial hypercholesterolemia (FH) heterozygotes. By extending genotype analysis to families of the index cases, we identified 12 mutation clusters and localized them in specific areas of Italy. To evaluate the impact of these mutations on the clinical expression of FH, the clusters...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1987
T L Innerarity K H Weisgraber K S Arnold R W Mahley R M Krauss G L Vega S M Grundy

Previous in vivo turnover studies suggested that retarded clearance of low density lipoproteins (LDL) from the plasma of some hypercholesterolemic patients is due to LDL with defective receptor binding. The present study examined this postulate directly by receptor binding experiments. The LDL from a hypercholesterolemic patient (G.R.) displayed a reduced ability to bind to the LDL receptors on...

Journal: :Revista espanola de cardiologia 2003
Ignacio García-Alvarez Sergio Castillo Pilar Mozas Diego Tejedor Gilberto Reyes Marta Artieda Ana Cenarro Rodrigo Alonso Pedro Mata Miguel Pocovi Fernando Civeira

INTRODUCTION AND OBJECTIVES Familial hypercholesterolemia and familial defective Apo B-100 are phenotypically indistinguishable. At present they can be distinguished by genetic analysis. PATIENTS AND METHODç We compared the clinical features of 13 subjects with familial defective Apo B-100 and 39 subjects with familial hypercholesterolemia. We used data from first degree relatives to compare mo...

Journal: :The Journal of Japan Atherosclerosis Society 1979

Journal: :Neurobiology of Aging 2013

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1993
W J Strittmatter A M Saunders D Schmechel M Pericak-Vance J Enghild G S Salvesen A D Roses

Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. In vitro, apolipoprotein E in cerebrospinal fluid binds to synthetic beta A4 peptide (the primary constituent of the senile plaque) with high avidity. Amino acids 12-28 of the beta A4 peptide are required. The gene for apolipoprotein E is located on chromosom...

Journal: :Circulation. Cardiovascular genetics 2011
Puneetpal Singh Mario Di Napoli Monica Singh

BACKGROUND In humans, the E4 allele of the apolipoprotein E gene is associated with increased coronary heart disease risk. Surprisingly, in rodents, apolipoprotein E4 only accelerates the atherosclerotic process when transgenic for the human low-density lipoprotein receptor (LDLR) protein. We therefore investigated whether the LDLR locus interacted with the apolipoprotein E gene genotype on cor...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید