関連する実験動画

Updated: Aug 17, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

ラトロゲン性リン酸枯渇による近接性ミオパシー

M Ravid, M Robson

    JAMA
    |September 20, 1976
    PubMed
    まとめ

    慢性腎不全患者のアルミニウム水酸化物ゲルは,低酸性血症による重度の骨髄病を引き起こす可能性があります. 抗酸性療法を中止し,リン酸補給を行うことで,患者の回復につながりました.

    さらに関連する動画

    Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag08:55

    Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag

    Published on: December 14, 2017

    Exon Skipping in Directly Reprogrammed Myotubes Obtained from Human Urine-Derived Cells06:20

    Exon Skipping in Directly Reprogrammed Myotubes Obtained from Human Urine-Derived Cells

    Published on: May 7, 2020

    関連する概念動画

    Protein Kinases and Phosphatases02:54

    Protein Kinases and Phosphatases

    Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
    Protein kinases
    Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
    Satellite Stem Cells and Muscular Dystrophy01:21

    Satellite Stem Cells and Muscular Dystrophy

    Satellite stem cells or myosatellite cells are quiescent stem cells that Alexander Mauro first identified in 1961. These cells are located between the sarcolemma, the plasma membrane of muscle fibers, and the basal lamina, the connective tissue sheath covering it. These mononucleated cells are activated in response to muscle injury, can transform into myoblasts, and may form or repair muscle fibers. Myosatellite cells can provide additional myonuclei for muscle regeneration or return to a...
    Myasthenia Gravis: Overview and Treatment01:20

    Myasthenia Gravis: Overview and Treatment

    Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
    These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
    Muscle Recovery and Fatigue01:24

    Muscle Recovery and Fatigue

    Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective response...
    Inborn Errors of Metabolism01:20

    Inborn Errors of Metabolism

    Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
    Myasthenia Gravis ll: Pathophysiology01:22

    Myasthenia Gravis ll: Pathophysiology

    The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...