Titlebook: Human Apolipoprotein Mutants; Impact on Atheroscle C. R. Sirtori,A. V. Nichols,G. Franceschini Book 1986 Springer Science+Business Media Ne

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書目名稱Human Apolipoprotein Mutants影響因子(影響力)




書目名稱Human Apolipoprotein Mutants影響因子(影響力)學(xué)科排名




書目名稱Human Apolipoprotein Mutants網(wǎng)絡(luò)公開度




書目名稱Human Apolipoprotein Mutants網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Human Apolipoprotein Mutants被引頻次




書目名稱Human Apolipoprotein Mutants被引頻次學(xué)科排名




書目名稱Human Apolipoprotein Mutants年度引用




書目名稱Human Apolipoprotein Mutants年度引用學(xué)科排名




書目名稱Human Apolipoprotein Mutants讀者反饋




書目名稱Human Apolipoprotein Mutants讀者反饋學(xué)科排名

Clinch

Apolipoprotein AI-Milano: A Structural Modification in an Apolipoprotein Variant Leading to Unusual emia, and premature atherosclerosis. By contrast, with the exception of the apo AI., there is no convincing evidence M associating any of the described apo AI variants with pathological conditions or with significant alterations of lipid and lipoprotein metabolism.

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Versatile , Expression-Modification Vectors as Tools for Structure-Function Studies of Apolipoprotei Nut.), and the ribosome binding site and initiation codon of the ell gene (Rosenberg et al., 1983). More recently, a derivative of pAS1 was described having the transcription termination signal t. positioned beyond the Bam H1 cloning site: this plasmid was named pOTS (Devare et al., 1984).

Electrolysis

The Function of Human Serum Apolipoproteins: Clues from Inborn Errors of Lipoprotein Metabolismated to a structural defect or a defect in the biosynthesis or secretion of apolipoproteins. Due to the numerous functions of serum apolipoproteins (Table 4), structural defects of these proteins potentially cause complex metabolic consequences.

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哀悼

Normal Genetic Lipoprotein Variations and Atherosclerosisinheritance or genetic predisposition. We are then confronted with the complex problem of interaction between environmental, nutritional or life style factors on the one hand and the individual’ s genotype on the other. Atherosclerotic disease, especially coronary heart disease (CHD) poses such a problem.

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Morphine

Recent Studies on the Metabolic Defect in Tangier Diseaselevels of apoA-I and apoA-II in Tangier disease are due to increased catabolism rather than reduced synthesis of the A-I and A-II apolipoproteins (5). In the present report, we will review our recent studies on the molecular defect in Tangier disease.

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