نتایج جستجو برای: familial hypercholesterolemia fh

تعداد نتایج: 68801  

Journal: :Atherosclerosis 2015
J M H Galema-Boers J Versmissen H W O Roeters van Lennep J E Dusault-Wijkstra M Williams J E Roeters van Lennep

PURPOSE This study assesses the success of the recently terminated Dutch nationwide cascade screening by examining whether children with familial hypercholesterolemia (FH) were identified through family screening or due to cardiovascular (CVD) events in the FH parent. METHODS We collected clinical information of all children (0-18 years) with FH with a pathogenic variant at our outpatient lip...

Journal: :Hypertension 2000
A S Wierzbicki M Lambert-Hammill P J Lumb M A Crook

The role of renin-angiotensin system polymorphisms as risk factors for coronary heart disease (CHD) is controversial. This study investigated their role in patients with heterozygous familial hypercholesterolemia (FH). Polymorphism frequencies for angiotensin-I-converting enzyme insertion/deletion (ACE I/D), angiotensinogen M235T, and angiotensin-II type I receptor (AG2R) A1166C were determined...

2018
Andrea De Lorenzo Juliana Duarte Lopes da Silva Cinthia E. James Alexandre C. Pereira Annie Seixas Bello Moreira

BACKGROUND Familial hypercholesterolemia (FH) is a common autosomal dominant disorder, characterized by a high level of low-density lipoprotein cholesterol (LDL-C) and a high risk of premature cardiovascular disease. OBJECTIVE To evaluate clinical and anthropometric characteristics of patients with the familiar hypercholesterolemia (FH) phenotype, with or without genetic confirmation of FH. ...

Journal: :Clinical chemistry 2001
E S Tai E S Koay E Chan T J Seng L M Loh S K Sethi C E Tan

BACKGROUND Familial hypercholesterolemia (FH) and familial defective apolipoprotein B-100 (FDB) represent ligand-receptor disorders that are complementary. Individuals with both FH and FDB are unusual. We report a family with both disorders and the impact of the mutations on the phenotypes of the family members. METHODS We used single strand conformation polymorphism (SSCP) and denaturing gra...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2010
Anouk van der Graaf Maud N Vissers Daniel Gaudet Diane Brisson Suthesh Sivapalaratnam Tessa J Roseboom Angelique C M Jansen John J P Kastelein Barbara A Hutten

OBJECTIVE It is unknown whether elevated maternal low-density lipoprotein cholesterol (LDL-C) levels lead to dyslipidemia in the offspring. Because this could have important consequences for cardiovascular prevention in mother and child, we explored the relationship between maternal familial hypercholesterolemia (FH) and lipids in adult offspring. METHODS AND RESULTS In a large cohort of both...

2017
Jiayin Yang Yu Wang Ting Zhou Lai-Yung Wong Xiao-Yu Tian Xueyu Hong Wing-Hon Lai Ka-Wing Au Rui Wei Yuqing Liu Lai-Hung Cheng Guichan Liang Zhijian Huang Wenxia Fan Ping Zhao Xiwei Wang David P. Ibañez Zhiwei Luo Yingying Li Xiaofen Zhong Shuhan Chen Dongye Wang Li Li Liangxue Lai Baoming Qin Xichen Bao Andrew P. Hutchins Chung-Wah Siu Yu Huang Miguel A. Esteban Hung-Fat Tse

Familial hypercholesterolemia (FH) causes elevation of low-density lipoprotein cholesterol (LDL-C) in blood and carries an increased risk of early-onset cardiovascular disease. A caveat for exploration of new therapies for FH is the lack of adequate experimental models. We have created a comprehensive FH stem cell model with differentiated hepatocytes (iHeps) from human induced pluripotent stem...

Journal: :Journal of lipid research 1998
P C Chan A Edwards R Lafrenière H G Parsons

In view of the presence of some 190 mutations in the low density lipoprotein receptor (LDL-R) gene and a lack of simple detection methods, we have developed an improved assay system for detecting familial hypercholesterolemia (FH) using mitogen-induced proliferating lymphocytes. Freshly isolated mononuclear cells were cultured for 3 days in RPMI 1640 supplemented with 10% human lipoprotein-defi...

Journal: :Arteriosclerosis and thrombosis : a journal of vascular biology 1993
P V Koivisto U M Koivisto P T Kovanen H Gylling T A Miettinen K Kontula

We describe a mutation of the low-density lipoprotein (LDL) receptor gene, designated familial hypercholesterolemia (FH)-Espoo, which deletes exon 15 of the LDL receptor gene. The mutant receptor is predicted to lack 57 amino acids, including 18 serine and threonine residues, which are the sites of the clustered O-linked sugars of the receptor. Studies on 10 carriers of this gene revealed that ...

Journal: :Journal of lipid research 1999
L Haddad I N Day S Hunt R R Williams S E Humphries P N Hopkins

Monogenically inherited hypercholesterolemia is most commonly caused by mutations at the low density lipoprotein receptor (LDLR) locus causing familial hypercholesterolemia (FH) or at the apolipoprotein B (APOB) locus causing the disorder familial defective apoB (FDB). Probands from 47 kindreds with a strict clinical diagnosis of FH were selected from the Cardiovascular Genetics Research Lipid ...

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