Quantitation of serum apolipoprotein A-I, A-II, B, C-II, C-III and E in healthy Japanese by turbidimetric immunoassay: Reference values, and age- and sex-related differences

Noma, Akio; Hata, Yutaka; Goto, Yuichiro

doi:10.1016/0009-8981(91)90106-m

Cited by 92 publications

(20 citation statements)

References 31 publications

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“…The reason for this sexrelated difference in CSF apo A-I concentration is unknown, and is the converse of the situation in plasma, where the apo A-I concentration in males is lower than in females. 24 The CSF apo A-I level was significantly elevated in patients with acute meningitis and returned to the control level during recovery, but CSF apo E level remained high, even at the convalescent stage. This different behavior in CSF concentrations between apo A-I and apo E may be due to their different origins.…”

Section: Discussionmentioning

confidence: 90%

Apo A-I and Apo E Concentrations in Cerebrospinal Fluids of Patients with Acute Meningitis

et al. 1998

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SUMMARY.It has been demonstrated that apolipoproteins found in cerebrospinal fluid (CSF) play an important role in lipid metabolism in the central nervous system (CNS). Previously we reported that CSF apo A-I levels increased with the severity of neurological damage in poliovirus-infected macaques. In the present study, apo A-I was quantitatively analysed in CSF from patients with or without neurological diseases. In controls, CSF apo A-I level was significantly higher in males; 3.83 (0.40) mg/L, mean (SEM) (n = 19) compared with females, 2.42 (0.26) mg/L (n= 23, P

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Section: Discussionmentioning

confidence: 90%

Apo A-I and Apo E Concentrations in Cerebrospinal Fluids of Patients with Acute Meningitis

et al. 1998

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“…The concentrations of apo A-I, A-Il, B, C-II, C-Ill, and E were determined by immunoturbidimetry as described (ApoAuto; Daiichi Chemical, Tokyo, Japan) (30). Intraassay and between assays CV for apolipoprotein measurements were less than 6%.…”

Section: Analytical Measurementsmentioning

confidence: 99%

Genetic cholesteryl ester transfer protein deficiency caused by two prevalent mutations as a major determinant of increased levels of high density lipoprotein cholesterol.

Inazu

Haraki²,

Yagi³

et al. 1994

J. Clin. Invest.

234

160

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Genetic determinants of HDL cholesterol (HDL-C) levels in the general population are poorly understood. We previously described plasma cholesteryl ester transfer protein (CETP) deficiency due to an intron 14 G(+l)-to-A mutation(Intl4 A) in several families with very high HDL-C levels in Japan. Subjects with HDL-C 100 mg/dl (n = 130) were screened by PCR single strand conformational polymorphism analysis of the CETP gene. Two other mutations were identified by DNA sequencing or primer-mediated restriction map modification of PCR products: a novel intron 14 splice donor site mutation caused by a T insertion at position +3 from the exonl4/intronl4 boundary (Intl4 T) and a missense mutation (Asp'2 to Gly) within exon 15 (D442G).The Intl4 T mutation was only found in one family. However, the D442G and Intl4 A mutations were highly prevalent in subjects with HDL-C . 60 mg/dl, with combined allele frequencies of 9%, 12%, 21%, and 43% for HDL-C 60-79, 80-99, 100-119, and . 120 mg/dl, respectively. Furthermore, prevalences of the D442G and Intl4 A mutations were extremely high in a general sample of Japanese men (n = 236), with heterozygote frequencies of 7% and 2%, respectively. These two mutations accounted for about 10% of the total variance of HDL-C in this population. The phenotype in a genetic compound heterozygote (Intl4 T and Intl4 A) was similar to that of Intl4 A homozygotes (no detectable CETP and markedly increased HDL-C), indicating that the Intl4 T produces a null allele. In four D442G homozygotes, mean HDL-C levels (86±26 mg/dl) were lower than in Intl4 A homozygotes (158±35 mgldl), reflecting residual CETP activity in plasma. In 47 D442G heterozygotes, mean HDL-C levels were 91±23 mg/dl, similar to the level in D442G homozygotes, and significantly greater than mean HDL-C levels in Intl4 A heterozygotes (69±15 mg/dl). Thus, the D442G mutation acts differently to the null mutations A portion of this paper was presented at the Asian-Pacific Congress on coronary heart disease risk factor held in Hong Kong, January 1994.

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“…19 Apolipoprotein levels were measured by immunoturbidimetry. 20 Vitamin A and K levels were determined by high-performance liquid chromatography 21,22 ; Vitamin E level was determined fluorometrically. 23 …”

Section: Serum Chemistry Analysesmentioning

confidence: 99%

Abetalipoproteinemia Caused by Maternal Isodisomy of Chromosome 4q Containing an Intron 9 Splice Acceptor Mutation in the Microsomal Triglyceride Transfer Protein Gene

Yang

Inazu

Yagi

et al. 1999

ATVB

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Abstract-Uniparental disomy (UPD), a rare inheritance of 2 copies of a single chromosome homolog or a region of a chromosome from one parent, can result in various autosomal recessive diseases. Abetalipoproteinemia (ABL) is a rare autosomal recessive deficiency of apoB-containing lipoproteins caused by a microsomal triglyceride transfer protein (MTP) deficiency. In this study, we describe a patient with ABL inherited as a homozygous intron 9 splice acceptor G(Ϫ1)-to-A mutation of the transfer protein gene. This mutation alters the splicing of the mRNA, resulting in a 36 amino acids, in-frame deletion of sequence encoded by exon 10. We analyzed chromosome 4, including MTP gene (4q22-24), using short tandem repeat markers. The proband has only his mother's genes in chromosome 4q spanning a 150-centimorgan region; ie, segmental maternal isodisomy 4q21-35, probably due to mitotic recombination. Nonpaternity between the proband and his father was excluded using 6 polymorphic markers from different chromosomes (paternity probability, 0.999). Maternal isodisomy (maternal UPD 4q) was the basis for homozygosity of the MTP gene mutation in this patient. (Arterioscler Thromb Vasc Biol. 1999;19

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Quantitation of serum apolipoprotein A-I, A-II, B, C-II, C-III and E in healthy Japanese by turbidimetric immunoassay: Reference values, and age- and sex-related differences

Cited by 92 publications

References 31 publications

Apo A-I and Apo E Concentrations in Cerebrospinal Fluids of Patients with Acute Meningitis

Apo A-I and Apo E Concentrations in Cerebrospinal Fluids of Patients with Acute Meningitis

Genetic cholesteryl ester transfer protein deficiency caused by two prevalent mutations as a major determinant of increased levels of high density lipoprotein cholesterol.

Abetalipoproteinemia Caused by Maternal Isodisomy of Chromosome 4q Containing an Intron 9 Splice Acceptor Mutation in the Microsomal Triglyceride Transfer Protein Gene

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