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 Experiment Videos

Familial polycythemia.

J W Adamson

    Seminars in Hematology
    |October 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

    Genetic defects can cause familial polycythemia by disrupting red blood cell production. Studying erythropoiesis regulation helps identify these distinct genetic causes and understand normal red cell physiology.

    Related Concept Videos

    You might also read

    Related Articles

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

    Sort by
    Same author

    The rate of marrow recovery and extent of donor engraftment following transplantation of ex vivo-expanded bone marrow cells are independently influenced by the cytokines used for expansion.

    Stem cells and development·2005
    Same author

    Murine bone marrow cells cultured ex vivo in the presence of multiple cytokine combinations lose radioprotective and long-term engraftment potential.

    Stem cells and development·2004
    Same author

    Placental/umbilical cord blood (PCB) stem cells for transplantation: early clinical outcomes and the status of ex vivo expansion strategies.

    The Keio journal of medicine·2001
    Same author

    Cell dose and speed of engraftment in placental/umbilical cord blood transplantation: graft progenitor cell content is a better predictor than nucleated cell quantity.

    Blood·2000
    Same author

    Identification of five new isoforms of murine thrombopoietin mRNA.

    Biochemical and biophysical research communications·2000
    Same author

    Identification of a glialblastoma cell differentiation factor-related gene mRNA in human microvascular endothelial cells.

    Genomics·2000
    Same journal

    Pain in SCD-Many mechanisms and mysteries.

    Seminars in hematology·2026
    Same journal

    The many facets of cardiopulmonary complications in sickle cell disease.

    Seminars in hematology·2026
    Same journal

    Clonal hematopoiesis in the setting of sickle cell disease and its relevance to curative therapies.

    Seminars in hematology·2026
    Same journal

    Treatment of myeloproliferative neoplasms: Exploring new horizons of who and when to cytoreduce in patients with polycythemia vera and essential thrombocytosis.

    Seminars in hematology·2026
    Same journal

    Telomeres biology disorders: the past, the present and the future.

    Seminars in hematology·2026
    Same journal

    Cardiovascular complications in patients with myeloproliferative neoplasms: What hematologists need to know.

    Seminars in hematology·2026
    See all related articles

    Area of Science:

    • Hematology
    • Genetics
    • Physiology

    Background:

    • Erythropoiesis (red blood cell production) is a complex process regulated at multiple steps.
    • Genetic defects can lead to familial polycythemia, a condition characterized by an abnormally high red blood cell count.
    • Understanding these defects requires examining marrow regulation and erythropoietin (ESF) production.

    Purpose of the Study:

    • To investigate how genetically determined defects cause familial polycythemia.
    • To characterize distinct patterns of marrow regulation associated with these defects.
    • To elucidate the physiological mechanisms underlying erythropoiesis regulation.

    Main Methods:

    • Physiological studies correlating erythropoietin (ESF) production, oxygen transport, and red cell production in affected individuals.

    Related Experiment Videos

  • Analyzing patterns of ESF production at rest and in response to altered oxygen supply.
  • Investigating defects in ESF production/release, renal oxygen sensing, and receptor function.

    • Main Results:

    • Distinct patterns of marrow regulation are associated with different genetic defects in erythropoiesis.
    • Defects in ESF production, oxygen sensing, or receptor function manifest as specific ESF production profiles.
    • These findings highlight the genetic control over various levels of red blood cell production regulation.

    Conclusions:

    • Multiple genetic defects can lead to familial polycythemia through distinct disruptions in erythropoiesis.
    • Characterizing ESF production patterns aids in dissecting genetically controlled regulatory levels.
    • Further research will enhance understanding of normal red blood cell production physiology.