Publications by authors named "G D Abbott"

Loss-of-function sequence variants in , which encodes the voltage-gated potassium channel Kv1.1, cause Episodic Ataxia Type 1 (EA1) and epilepsy. Due to a paucity of drugs that directly rescue mutant Kv1.

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Two-pore domain, outwardly rectifying potassium (TOK) channels are exclusively expressed in fungi. Human fungal pathogen TOK channels are potential antifungal targets, but TOK channel modulation in general is poorly understood. Here, we discovered that TOK (CaTOK) is regulated by extracellular pH, in contrast to TOK channels from other fungal species tested.

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Background: This study examined (1) associations between sociodemographic and clinical variables with low muscle mass and radiodensity and their loss relative to treatment commencement in patients with lung cancer; and (2) the magnitude of change in muscle mass and association with treatment outcomes and survival.

Methods: Prospective study in patients planned for curative (chemo)radiotherapy for lung cancer. Low skeletal muscle mass and radiodensity and muscle loss were determined from pre- and post-treatment computed tomography images.

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Human voltage-gated potassium (Kv) channels are expressed by a 40-member gene family that is essential for normal electrical activity and is closely linked to various excitability disorders. Function-altering sequence variants in the gene, which encodes the neuronally expressed Kv2.1 channel, are associated with neurodevelopmental disorders including developmental delay with or without epileptic activity.

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Plants remain an important source of biologically active small molecules with high therapeutic potential. The voltage-gated potassium (Kv) channel formed by Kv7.2/3 (KCNQ2/3) heteromers is a major target for anticonvulsant drug development.

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