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Optimized Negative Staining: a High-throughput Protocol for Examining Small and Asymmetric Protein Structure by Electron Microscopy

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[Apolipoprotein B and small, dense LDL-C].

¹Reagent R&D Department, Denka Seiken Co., Ltd. Gosen, 959-1695, Japan. y_ito@denka-seiken.co.jp

Rinsho Byori. the Japanese Journal of Clinical Pathology

|June 13, 2012

Summary

Apolipoprotein B-100 (apo B-100) and small, dense LDL-C (sdLDL-C) are key markers for coronary heart disease (CHD) risk. Measuring both provides deeper insights into CHD causes and guides personalized treatment strategies.

Area of Science:

Cardiovascular Medicine
Clinical Chemistry
Lipidology

Background:

Coronary heart disease (CHD) risk is significantly influenced by lipid profiles.
Apolipoprotein B-100 (apo B-100) and small, dense LDL-C (sdLDL-C) are established biomarkers for CHD.
Elevated levels of these markers are associated with conditions like familial hypercholesterolemia, familial combined hyperlipidemia, diabetes mellitus, and metabolic syndrome.

Purpose of the Study:

To evaluate the clinical utility of apo B-100 and sdLDL-C as risk markers for CHD.
To investigate the differential diagnostic value of apo B-100 and sdLDL-C in various hyperlipidemic conditions.
To determine if combined assessment of apo B-100 and sdLDL-C offers enhanced clinical information for CHD risk stratification.

Main Methods:

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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation

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Apo B-100 was measured using a fully automated turbidimetric immunoassay.
SdLDL-C was quantified via an enzymatic homogeneous assay on an automated analyzer.
Comparative analysis of apo B-100 and sdLDL-C levels was performed across different patient groups.

Main Results:

Both apo B-100 and sdLDL-C are independently associated with increased CHD risk.
Distinct patterns of apo B-100 and sdLDL-C elevation were observed: familial hypercholesterolemia showed higher apo B-100, while diabetes mellitus and metabolic syndrome showed higher sdLDL-C.
Familial combined hyperlipidemia exhibited similar levels for both markers.
Combined assessment revealed nuanced differences in marker tendencies across conditions.

Conclusions:

Measuring both apo B-100 and sdLDL-C provides complementary information for CHD risk assessment.
The differential elevation patterns of these markers can help elucidate the underlying cause of CHD.
Combined analysis enhances clinical utility, potentially leading to more targeted and effective patient treatments.