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channelopathies/demam
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Managing pregnancy and anaesthetics in patients with skeletal muscle channelopathies
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The skeletal muscle channelopathies are a group of rare diseases and include non-dystrophic myotonia and periodic paralysis. Given their rarity, little has been published on the management of anaesthesia and pregnancy in this cohort despite being important aspects of care. We have conducted a large
[Ion channel abnormalities ("channelopathies") in neurologic diseases].
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THE ROLE OF IONIC CHANNEL DYSFUNCTION: During various neurological diseases has been evoked for many years on electro-physiological data. Molecular biology has led to great progress in neurology, and can be considered "functional" since it is surpasses the classical anatomo-clinical methods. IONIC
L-type Ca2+ channels in Ca2+ channelopathies.
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Voltage-gated L-type Ca2+ channels (LTCCs) mediate depolarization-induced Ca2+ entry in electrically excitable cells, including muscle cells, neurons, and endocrine and sensory cells. In this review we summarize the role of LTCCs for human diseases caused by genetic Ca2+ channel defects
Neurological channelopathies: diagnosis and therapy in the new millennium.
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Rapid progress in the complementary fields of molecular genetics and cellular electrophysiology has led to a better understanding of many disorders which are caused by ion channel dysfunction. These channelopathies may manifest in a multitude of ways depending on the tissue specificity of the
Channelopathies in Cav1.1, Cav1.3, and Cav1.4 voltage-gated L-type Ca2+ channels.
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Voltage-gated Ca2+ channels couple membrane depolarization to Ca2+-dependent intracellular signaling events. This is achieved by mediating Ca2+ ion influx or by direct conformational coupling to intracellular Ca2+ release channels. The family of Cav1 channels, also termed L-type Ca2+ channels
[Channelopathy].
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Recently, a variety of ion channel defects have been identified as the biological basis of certain familial epilepsies, paroxysmal movement disorders, myopathies and some degenerative disorders of central nervous system. Ion channel defects were mainly caused by genetic and autoimmune mechanisms.
Fever Unmasked Brugada Syndrome in Pediatric Patient: A Case Report
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Introduction: Brugada syndrome is an arrhythmogenic disorder that is a known cause of sudden cardiac death. It is characterized by a pattern of ST segment elevation in the precordial leads on an electrocardiogram (EKG) due to a sodium
Skeletal muscle channelopathies.
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Ion channelopathies have common clinical features, recurrent patterns of mutations, and almost predictable mechanisms of pathogenesis. In skeletal muscle, disorders are associated with mutations in voltage-gated Na(+), K(+), Ca(2+), and Cl(-) channels leading to hypoexcitability, causing periodic
Disorders of membrane channels or channelopathies.
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OBJECTIVE
To review the structure and function of membrane ion channels with special emphasis on inherited nervous system channel disorders or channelopathies.
RESULTS
Channels are pores in the cell membrane. Through these pores ions flow across the membrane and depolarize or hyperpolarize the cell.
State of the art in hereditary muscle channelopathies.
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A combination of electrophysiological and genetic studies has resulted in the identification of several skeletal muscle disorders to be caused by pathologically functioning ion channels and has led to the term channelopathies. Typical hereditary muscle channelopa thies are congenital myasthenic
Muscle biopsy and cell cultures: potential diagnostic tools in hereditary skeletal muscle channelopathies.
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Hereditary muscle channelopathies are caused by dominant mutations in the genes encoding for subunits of muscle voltage-gated ion channels. Point mutations on the human skeletal muscle Na+ channel (Nav1.4) give rise to hyperkalemic periodic paralysis, potassium aggravated myotonia, paramyotonia
[Channelopathies in neurology].
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BACKGROUND
The main function of ionic channels are the conduction, recognition and selection of specific ions. They open and close in respond answer to electrical, mechanical and chemical stimulus, acting in the excitation or transmission of diverse tissues.
METHODS
The clinical and molecular
A pediatric case of Brugada syndrome diagnosed by fever-provoked ventricular tachycardia.
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Brugada syndrome is a rare channelopathy associated with the SCN5A gene that causes fatal ventricular arrhythmias. This case of Brugada syndrome, in which ventricular tachycardia (VT) was provoked by high fever, is the first report in a Korean child. The boy had retinoblastoma of his left eye
Unusual perianesthetic malignant hyperthermia in a dog.
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METHODS
A 7-month-old male Siberian Husky affected by lower motor neuron tetraparesis was anesthetized for electrodiagnostic testing and collection of muscle and nerve biopsy specimens.
RESULTS
Preanesthetic physical examination revealed a high rectal temperature, and serum biochemical analysis
Malignant hyperthermia: clinical and molecular aspects.
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BACKGROUND
Malignant hyperthermia (MH) is a potentially lethal pharmacogenetic disorder that affects genetically predisposed individuals. It manifests in susceptible individuals in response to exposure to Inhalant anesthetics, depolarizing muscle relaxants or extreme physical activity in hot
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