نتایج جستجو برای: familial defective apolipoprotein

تعداد نتایج: 117246  

Journal: :Brain : a journal of neurology 2014
Mitsuru Shinohara Shinsuke Fujioka Melissa E Murray Aleksandra Wojtas Matthew Baker Anne Rovelet-Lecrux Rosa Rademakers Pritam Das Joseph E Parisi Neill R Graff-Radford Ronald C Petersen Dennis W Dickson Guojun Bu

Recent studies suggest that subcortical structures, including striatum, are vulnerable to amyloid-β accumulation and other neuropathological features in familial Alzheimer's disease due to autosomal dominant mutations. We explored differences between familial and sporadic Alzheimer's disease that might shed light on their respective pathogenic mechanisms. To this end, we analysed 12 brain regio...

Journal: :The Journal of clinical investigation 1980
R J Havel L Kotite J L Vigne J P Kane P Tun N Phillips G C Chen

A radioimmunoassay for apolipoprotein E in human blood serum has been developed that measures equally the major polymorphic species of the protein (apolipoproteins E-1, E-2, E-3, and E-4) and the apo E in the dimer of apolipoproteins E and A-II. The assay is specific and yields values for apolipoprotein E in very low density lipoproteins that agree closely with those obtained by a quantitative ...

ژورنال: Medical Laboratory Journal 2012
Alizadeh Sharg Sh, , Dolatkhah H, , Movahedian A, , Rahmani S Z, ,

Abstract Background and objectives: Familial hypercholesterolemia (FH) is an autosomal disorder characterized by increased levels of total cholesterol and low density lipoprotein cholesterol. The FH clinical phenotype has been associated with increased risk of coronary heart disease and premature death. The mutation in LDLR gene in most cases is responsible for FH phenotype. Furthermore, other ...

Journal: :Science 1997
L Masucci-Magoulas I J Goldberg C L Bisgaier H Serajuddin O L Francone J L Breslow A R Tall

Familial combined hyperlipidemia (FCHL) is a common inherited lipid disorder, affecting 1 to 2 percent of the population in Westernized societies. Individuals with FCHL have large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) and develop premature coronary heart disease. A mouse model displaying some of the features of FCHL was created by crossing mice carr...

2014
Mitsuru Shinohara Shinsuke Fujioka Melissa E. Murray Aleksandra Wojtas Matthew Baker Anne Rovelet-Lecrux Rosa Rademakers Pritam Das Joseph E. Parisi Neill R. Graff-Radford Ronald C. Petersen Dennis W. Dickson Guojun Bu

Recent studies suggest that subcortical structures, including striatum, are vulnerable to amyloid-b accumulation and other neuropathological features in familial Alzheimer’s disease due to autosomal dominant mutations. We explored differences between familial and sporadic Alzheimer’s disease that might shed light on their respective pathogenic mechanisms. To this end, we analysed 12 brain regio...

Journal: :Atherosclerosis 2000
Y N Teng J P Pan S C Chou D Y Tai G J Lee-Chen

Familial defective apolipoprotein (apo) B-100 (FDB) is caused by R3500Q mutation of the apo B gene resulting in decreased binding of LDL to the LDL receptor. Two other apo B mutations, R3500W and R3531C, affecting binding are known to date. We screened the apo B gene segment around codon 3500 by heteroduplex analysis and single strand conformation polymorphism (SSCP) analysis in a total of 373 ...

Journal: :Arteriosclerosis and thrombosis : a journal of vascular biology 1994
P S Hansen H Meinertz H K Jensen P Fruergaard J Launbjerg I C Klausen L Lemming U Gerdes N Gregersen O Faergeman

Plasma concentrations of cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo) B, and lipoprotein(a) (Lp[a]) in 46 persons heterozygous for the apo B-3500 mutation causing familial defective apo B-100 (FDB) were compared with those in 57 non-FDB relatives. FDB patients had 50% to 70% higher mean concentrations of cholesterol, LD...

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