Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

RNA Editing02:23

RNA Editing

RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cross-cultural comparisons between Taipei Chinese and Framingham Americans: dietary intakes, blood lipids and apolipoproteins.

Asia Pacific journal of clinical nutrition·2013
Same author

Plasma proprotein convertase subtilisin kexin type 9 levels are related to markers of cholesterol synthesis in familial combined hyperlipidemia.

Nutrition, metabolism, and cardiovascular diseases : NMCD·2013
Same author

Short communication: Effects of different whey concentrations on physicochemical characteristics and viable counts of starter bacteria in dairy beverage supplemented with probiotics.

Journal of dairy science·2012
Same author

Utility of glycated albumin for the diagnosis of diabetes mellitus in a Japanese population study: results from the Kyushu and Okinawa Population Study (KOPS).

Diabetologia·2011
Same author

Effects of margarines and butter consumption on lipid profiles, inflammation markers and lipid transfer to HDL particles in free-living subjects with the metabolic syndrome.

European journal of clinical nutrition·2010
Same author

Genetic variation at the hormone sensitive lipase: gender-specific association with plasma lipid and glucose concentrations.

Clinical genetics·2004
Same journal

Extracellular matrix reprogramming by the YAP/TAZ- TGF-ß2 axis drives immune exclusion in cholangiocarcinoma models.

The Journal of clinical investigation·2026
Same journal

Tumor cell-derived extracellular vesicles foster the immunosuppressive landscape of pancreatic cancer.

The Journal of clinical investigation·2026
Same journal

Julie Zikherman receives the ASCI/Marian W. Ropes, MD, Award.

The Journal of clinical investigation·2026
Same journal

Targeted degradation of MDM2 overcomes feedback regulation of p53 signaling in Merkel cell carcinoma models.

The Journal of clinical investigation·2026
Same journal

SGLT2 inhibitors enhance ketogenesis by acting as allosteric activators of the mitochondrial enzyme HMGCS2.

The Journal of clinical investigation·2026
Same journal

MDM2 degraders for Merkel cell carcinoma: round peg in a round hole.

The Journal of clinical investigation·2026
See all related articles

Related Experiment Video

Updated: Jun 8, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Familial apolipoprotein E deficiency.

E J Schaefer, R E Gregg, G Ghiselli

    The Journal of Clinical Investigation
    |November 1, 1986
    PubMed
    Summary
    This summary is machine-generated.

    Familial apolipoprotein E deficiency causes type III hyperlipoproteinemia. This condition severely impairs the body's ability to process lipoproteins, leading to premature cardiovascular disease.

    More Related Videos

    Quantification of Atherosclerosis in Mice
    06:59

    Quantification of Atherosclerosis in Mice

    Published on: June 12, 2019

    High-Density Lipoprotein-Specific Phospholipid Efflux Assay
    07:08

    High-Density Lipoprotein-Specific Phospholipid Efflux Assay

    Published on: September 30, 2025

    Related Experiment Videos

    Last Updated: Jun 8, 2026

    Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
    07:36

    Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

    Published on: September 26, 2018

    Quantification of Atherosclerosis in Mice
    06:59

    Quantification of Atherosclerosis in Mice

    Published on: June 12, 2019

    High-Density Lipoprotein-Specific Phospholipid Efflux Assay
    07:08

    High-Density Lipoprotein-Specific Phospholipid Efflux Assay

    Published on: September 30, 2025

    Area of Science:

    • Genetics
    • Metabolic Disorders
    • Cardiovascular Science

    Background:

    • Familial apolipoprotein E (apoE) deficiency is a rare genetic disorder.
    • Type III hyperlipoproteinemia (HLP) is characterized by elevated cholesterol and triglyceride levels.
    • Premature cardiovascular disease and tubo-eruptive xanthomas are clinical manifestations.

    Observation:

    • A unique kindred with premature cardiovascular disease and type III HLP was studied.
    • Homozygotes exhibited marked increases in cholesterol-rich very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL).
    • Homozygotes had trace amounts of plasma apoE and accumulations of apoB-48 and apoA-IV in lipoproteins.

    Findings:

    • Homozygous familial apoE deficiency leads to type III HLP.
    • Markedly decreased apoE production and severely retarded catabolism of VLDL apoB and plasma apoE were observed in homozygotes.
    • Obligate heterozygotes had normal plasma lipids with approximately 42% of normal plasma apoE concentrations.

    Implications:

    • Apolipoprotein E is essential for the normal catabolism of triglyceride-rich lipoproteins.
    • Understanding apoE's role is crucial for managing hyperlipoproteinemia and cardiovascular disease.
    • Diet and medications like niacin and clofibrate can help manage lipid levels in affected individuals.