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

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters01:16

Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...
Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...

You might also read

Related Articles

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

Sort by
Same author

Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.

Diagnostics (Basel, Switzerland)·2026
Same author

Special Issue: "Molecular Mechanisms and Regulation in Chronic Kidney Diseases".

International journal of molecular sciences·2026
Same author

The Ethical Aspects of AI in Scientific Publishing.

EJIFCC·2026
Same author

Pharmacological treatment of presbyopia.

Acta clinica Belgica·2026
Same author

Validation study of the Helena V8 UltraCE capillary elecrophoresis analyser.

Clinical chemistry and laboratory medicine·2026
Same author

Vitamin D binding protein polymorphism is associated with body weight in females.

Hormone molecular biology and clinical investigation·2025

Related Experiment Video

Updated: Jul 2, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Haptoglobin polymorphism and lacunar stroke.

Julie Staals1, Barbe M A Pieters, Iris L H Knottnerus

  • 1Department of Neurology, University Hospital Maastricht, the Netherlands. j.staals@neurologie.azm.nl.

Current Neurovascular Research
|August 12, 2008
PubMed
Summary
This summary is machine-generated.

Haptoglobin (Hp) 1 allele is linked to a higher risk of lacunar stroke, a type of cerebrovascular disease. This finding suggests Hp polymorphism plays a role in brain small vessel disease, differing from its known vascular effects elsewhere.

More Related Videos

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats
06:39

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats

Published on: October 17, 2018

Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage
09:41

Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage

Published on: July 3, 2014

Related Experiment Videos

Last Updated: Jul 2, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats
06:39

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats

Published on: October 17, 2018

Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage
09:41

Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage

Published on: July 3, 2014

Area of Science:

  • Genetics
  • Neurology
  • Vascular Biology

Background:

  • Haptoglobin (Hp) 2-2 phenotype is linked to vascular complications in diabetes and peripheral artery disease.
  • The association between Hp polymorphism and cerebrovascular disease remains unexplored.
  • Lacunar stroke, a type of stroke caused by small vessel disease, is the focus of this study.

Purpose of the Study:

  • To investigate the association between Haptoglobin (Hp) polymorphism and lacunar stroke.
  • To compare Hp phenotypes in patients with first symptomatic lacunar stroke and a control group.
  • To explore potential mechanisms linking Hp to cerebral small vessel disease.

Main Methods:

  • Starch gel electrophoresis was used to determine Haptoglobin (Hp) phenotypes.
  • A case-control study design was employed with 124 lacunar stroke patients and 918 controls.
  • Analysis included Hp allele frequencies and phenotype distributions, with subgroup analysis for younger patients and those with concomitant lesions.

Main Results:

  • The Hp1 allele frequency was significantly higher in lacunar stroke patients (0.480) compared to controls (0.395).
  • The Hp2-2 phenotype was less frequent in patients (25.0%) than in controls (36.3%), indicating a protective association (OR 0.59).
  • This association was more pronounced in younger patients (age ≤60 years) and weakened in the presence of concomitant cerebral small vessel disease signs.

Conclusions:

  • Haptoglobin (Hp) 1 allele is associated with an increased risk of lacunar stroke, suggesting a role in cerebral small vessel disease.
  • The findings imply Hp may have organ-specific functions in vascular pathology.
  • Potential mechanisms include effects on blood-brain barrier integrity, hypertension association, or small vessel angiogenesis, with Hp phenotype playing a differential role based on underlying pathophysiology.