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  • JAMA December 17, 2014

    Figure 3: Effect of Study Diets on Main Outcomes

    The primary outcomes were systolic blood pressure, insulin sensitivity, and levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides. Diastolic blood pressure was a secondary outcome. Additional data related to these outcomes are presented in Table 3 and eTable 3 in Supplement 2. Apolipoproteins and other lipid outcomes are in eTable 4. Carb indicates carbohydrate; GI, glycemic index. To convert cholesterol to mmol/L, multiply by 0.0259; triglycerides to mmol/L, multiply by 0.0113.aFor the 5 primary outcomes on the primary diet contrast (insulin sensitivity, triglycerides, HDL cholesterol, LDL cholesterol, and systolic blood pressure), we plot and tabulate 99% CI to achieve nominal 95% coverage.
  • Association of LDL Cholesterol, Non–HDL Cholesterol, and Apolipoprotein B Levels With Risk of Cardiovascular Events Among Patients Treated With Statins: A Meta-analysis

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    JAMA. 2012; 307(12):1302-1309. doi: 10.1001/jama.2012.366
  • JAMA March 28, 2012

    Figure 1: Association Between on-Statin Lipid or Apolipoprotein Levels and Risk of Major Cardiovascular Events Stratified by Baseline Characteristics

    Data markers indicate hazard ratios for risk of major cardiovascular events per 1-SD increase of the lipid or apolipoprotein and 95% CIs. Dashed line indicates point estimate for all participants combined. All interaction terms were by presence or absence of the listed characteristics and were nonsignificant. BMI indicates body mass index; CHD, coronary heart disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; and TG, triglyceride.
  • JAMA March 28, 2012

    Figure 2: Association Between on-Statin Lipid or Apolipoprotein Levels and Risk of Major Cardiovascular Events Stratified by Study

    Data markers indicate hazard ratios (HRs) for risk of major cardiovascular events per 1-SD increase of on-statin low-density lipoprotein cholesterol (LDL-C), non–high-density lipoprotein cholesterol (non–HDL-C), or apolipoprotein B (apoB) and 95% CIs. For placebo-controlled trials, data from the placebo group were not used in this analysis. Dashed line indicates point estimate for all participants combined. All interaction terms by study were nonsignificant.
  • Major Lipids, Apolipoproteins, and Risk of Vascular Disease

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    JAMA. 2009; 302(18):1993-2000. doi: 10.1001/jama.2009.1619
  • JAMA November 11, 2009

    Figure 3: Hazard Ratios for Coronary Heart Disease Across Fifths of Usual Lipids or Apolipoproteins

    Analyses were based on 91 307 participants (involving 4499 cases) from 22 studies. Regression analyses were stratified, where appropriate, by sex and trial group and adjusted for age, systolic blood pressure, smoking status, history of diabetes mellitus, and body mass index; furthermore, analyses of non–HDL-C were adjusted for HDL-C and loge triglyceride, analyses of apolipoprotein B (apo B) were adjusted for apolipoprotein AI (apo AI) and loge triglyceride, analyses of HDL-C were adjusted for non–HDL-C and loge triglyceride, and analyses of apo AI were adjusted for apo B and loge triglyceride. Studies with fewer than 10 cases were excluded from analysis. Sizes of data markers are proportional to the inverse of the variance of the hazard ratios. Referent groups are lowest fifths. Lines are fitted by first-degree fractional polynomial regression of log hazard ratios on mean SD score. Error bars indicate 95% confidence intervals. The y-axis is shown on a log scale. The x-axis is shown on a Z-transformed scale.
  • JAMA June 10, 2009

    Figure 2: Mean Lipoprotein(a) Levels in the CCHS as a Function of Octiles or Quartiles of Apolipoprotein(a) KIV-2 Repeats

    P values are for Cuzick nonparametric test for trend of mean lipoprotein(a) levels. Participants in the 1991-1994 or 2001-2003 examination were included (n = 9867). CCHS indicates Copenhagen City Heart Study; KIV-2, kringle IV type 2. Error bars indicate 95% confidence intervals.
  • JAMA June 10, 2009

    Figure 3: Risk of Myocardial Infarction by Quartiles of Apolipoprotein(a) KIV-2 Repeats in the CCHS, CGPS, and CIHDS

    In the Copenhagen City Heart Study (CCHS), risk estimates were adjusted for age and sex or multivariably for age, sex, total cholesterol (corrected for the lipoprotein[a] contribution), triglycerides, body mass index, hypertension, diabetes mellitus, smoking, and use of lipid-lowering therapy and for women also for menopause and hormone therapy. In the Copenhagen General Population Study (CGPS) and Copenhagen Ischemic Heart Disease Study (CIHDS), odds ratios (ORs) were adjusted for age and sex or multivariably for age, sex, and diabetes mellitus. P values are test for trend of risk estimates (hazard ratios [HRs] or ORs) where kringle IV type 2 (KIV-2) groups with decreasing numbers of KIV-2 repeats were coded 1, 2, 3, and 4. There was no overlap of individuals between studies. Participants in the CGPS with incomplete information on covariates were dropped from analysis (n = 151); otherwise, numbers of individuals included are as shown in Table 1. CI indicates confidence interval (shown as error bars).
  • JAMA June 18, 2008

    Figure 2: Associations of CETP Genotypes With CETP Phenotypes and Lipid Levels

    CETP indicates cholesteryl ester transfer protein; CI, confidence interval; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol. To convert apolipoproteins A-I and B to mg/dL, divide by 0.01; to convert HDL-C and LDL-C to mg/dL, divide by 0.0259; and to convert triglyercides to mg/dL, divide by 0.0113. Assessment of heterogeneity: I2 (95% CI) for CETP mass, CETP activity, HDL-C, apolipoprotein A-I, LDL-C, apolipoprotein B, and triglycerides, respectively, were 66% (39%-81%), 71% (44%-86%), 75% (69%-80%), 66% (46%-78%), 51% (32%-65%), 14% (0%-51%), and 49% (30%-62%) for TaqIB; 0% (0%-71%), NA*, 56% (33%-71%), 0% (0%-68%), 24% (0%-58%), 16% (0%-60%), and 0% (0%-49%) for I405V; and 71% (17%-90%), NA*, 37% (0%-61%), 36% (0%-78%), 29% (0%-63%), 0% (0%-90%), and 0% (0%-57%) for −629C>A. NA* indicates I2 statistics were not calculated when there were only 2 studies. aPooled estimates calculated by random-effects models. Estimates calculated by fixed-effect models are shown in eTable 3. bStandardized mean differences. cCalculated with reference to the weighted mean level of each marker in common homozygotes.
  • Clinical Utility of Different Lipid Measures for Prediction of Coronary Heart Disease in Men and Women

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    JAMA. 2007; 298(7):776-785. doi: 10.1001/jama.298.7.776
  • JAMA August 15, 2007

    Figure 2: Overview of Reverse Cholesterol Transport and High-Density Lipoprotein Metabolism

    ABCA1 indicates adenosine triphosphate–binding cassette transporter A1; ABCG1, adenosine triphosphate–binding cassette transporter G1; apo, apolipoprotein; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LDL-R, LDL receptor; LPL, lipoprotein lipase; SR-B1, scavenger receptor type B1; VLDL, very low-density lipoprotein.
  • Lipoprotein(a), Measured With an Assay Independent of Apolipoprotein(a) Isoform Size, and Risk of Future Cardiovascular Events Among Initially Healthy Women

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    JAMA. 2006; 296(11):1363-1370. doi: 10.1001/jama.296.11.1363
  • Non–HDL Cholesterol, Apolipoproteins A-I and B 100 , Standard Lipid Measures, Lipid Ratios, and CRP as Risk Factors for Cardiovascular Disease in Women

    Abstract Full Text
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    JAMA. 2005; 294(3):326-333. doi: 10.1001/jama.294.3.326
  • JAMA July 20, 2005

    Figure 2: Probability of Cardiovascular Events According to Increasing Quintiles of Lipid, Apolipoprotein, and C-Reactive Protein Levels

    According to increasing quintiles of each measured variable over the 10-year follow-up period.
  • A Large High-Density Lipoprotein Enriched in Apolipoprotein C-I: A Novel Biochemical Marker in Infants of Lower Birth Weight and Younger Gestational Age

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    JAMA. 2005; 293(15):1891-1899. doi: 10.1001/jama.293.15.1891
  • JAMA April 20, 2005

    Figure 2: MALDI-TOF Mass Spectrometry of Apo C-I–Enriched HDL and Normal HDL

    Apo indicates apolipoprotein; MALDI-TOF, matrix-assisted laser desorption/ionization time-of-flight; and HDL, high-density lipoprotein. Apo C-I–enriched HDL (A and B) and normal HDL (C and D) were isolated from plasma of a group 0 infant (A and C) and a group 3 infant (B and D) and prepared for MALDI-TOF mass spectrometry (see “Methods” section).
  • JAMA March 16, 2005

    Figure: Theoretical Mechanism of Antioxidant Influence on Lipid Metabolism

    The nuclear receptor heterodimer RXR-LXR modulates the expression of key gene products (apolipoproteins, transporters, or enzymes) affecting lipid metabolism, via an upstream hormone response element DR4. RXR is activated by 9-cis retinoic acid and LXR by certain nuclear oxysterols. By affecting these sites of gene regulation, antioxidants could alter lipoprotein metabolism and lipid levels as has been observed. For example, isomers of vitamin A (retinoic acid), the breakdown product of beta carotene, could interfere with binding of the specific activator 9-cis retinoic acid to RXR; and antioxidants, including vitamin E, might alter oxysterol levels or their interaction with the LXR nuclear receptor by as yet unproven mechanisms. RXR indicates retinoid x receptor; LXR, liver x receptor; DR, direct repeat; Apo, apolipoprotein; ABC, ATP-binding cassette transmembrane protein; CETP, cholesterol ester transfer protein; SREBP, sterol regulatory element-binding protein.
  • Effect of a High-Fat Ketogenic Diet on Plasma Levels of Lipids, Lipoproteins, and Apolipoproteins in Children

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    JAMA. 2003; 290(7):912-920. doi: 10.1001/jama.290.7.912
  • JAMA November 14, 2001

    Figure 3: Prominent Differentiating Features in the Domain Architectures of Representative Human Proteins

    A protein domain is a structural and functional unit that shows evolutionary conservation and, by convention, is represented as a distinct geometric shape. Thus, proteins are made up of 1 or more such building blocks or "domains" and, depending on the types and numbers of domains, proteins with different biological capabilities are created. Many of these domains have seemingly arbitrary nomenclature that, in many cases, reflects the experimental nuances of their initial description. A library of curated protein domains with their biological descriptions is available through the Pfam and SMART databases.A, The extensive domain shuffling seen in the plasma proteases of the coagulation and complement systems. The "ancient" trypsin family serine protease domain occurs in combination with a myriad of protein interaction domains. Most of these domains are evolutionarily ancient, that is, with the exception of the Gla domain (see below); they are also observed in the fly and the worm. These include: (1) AP: Apple, originally described in the coagulation factors, predicted to possess protein- and/or carbohydrate-binding functions; (2) Kr: Kringle, named after a Danish pastry, has an affinity for lysine-containing peptides; (3) E: epidermal growth factor (EGF)-like; (4) CUB: domain first described in complement proteins and a diverse group of developmental proteins; (5) CCP: complement control protein repeats, also known as "sushi" repeats, first recognized in the complement proteins; and (6) Gla: a hyaluron-binding domain, contains γ-carboxyglutamate residues, and is seen in proteins associated with the extracellular matrix. Of note is the observation that apolipoprotein (a) likely represents a primate-specific evolutionary event. There is a tremendous expansion of the Kringle domain (dashed segment represents a total of 29 copies of the Kringle domain) in a trypsin family serine protease.B, Examples of domain accretion in nuclear regulators in the human compared with the fly. Domain accretion refers to greater numbers of a specific domain in a multidomain protein or addition of new domains to a multidomain protein. These domains include: (1) BTB: broad-complex, tramtrack, and bric-a-brac (a name that reflects its early descriptions in Drosophila), a protein interaction domain; (2) Zf: C2H2 class of DNA-binding zinc finger; (3) KRAB: Kruppel-associated box, a vertebrate-specific nuclear protein interaction domain; (4) HD: histone deacetylase, an important class of chromatin-modifying enzymes; (5) U: ubiquitin finger, a domain that targets proteins for proteolytic degradation. There is a major expansion of the numbers of C2H2 zinc fingers in the BTB or KRAB transcription factor (dashed segment represents a total of 3 copies of the Zf domain) families in the human, a feature that may reflect increased ability to mediate regulatory interactions with DNA.
  • JAMA July 7, 1999

    Figure 1: Atherosclerosis and APOE Genotype

    The relative mean wall thickness of the common carotid and internal carotid arteries according to apolipoprotein APOE ∊4 genotype. The referent is the mean artery wall thickness in APOE 2/2.