Dataset Information

Endoscopic Fusion of the Accessory Navicular Synchondrosis That Has No Diastasis.

ABSTRACT: Accessory navicular bone is a common accessory ossicle of the foot and is present in 10% to 14% of normal feet. Less than 1% of the accessory navicular bones are symptomatic. Degenerative or traumatic disruption of the accessory navicular synchondrosis is one of the main causes of symptomatic accessory navicular. The disrupted synchondrosis may or may not be associated with diastasis of the synchondrosis. Fusion of the synchondrosis is indicated if the pain fails to respond to conservative measures. The purpose of this Technical Note is to describe a minimally invasive approach for fusion of the synchondrosis that has no diastasis.

SUBMITTER: Lui TH

PROVIDER: S-EPMC5442306 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature

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Publications

Endoscopic Fusion of the Accessory Navicular Synchondrosis That Has No Diastasis.

Lui Tun Hing TH

Arthroscopy techniques 20170306 2

Accessory navicular bone is a common accessory ossicle of the foot and is present in 10% to 14% of normal feet. Less than 1% of the accessory navicular bones are symptomatic. Degenerative or traumatic disruption of the accessory navicular synchondrosis is one of the main causes of symptomatic accessory navicular. The disrupted synchondrosis may or may not be associated with diastasis of the synchondrosis. Fusion of the synchondrosis is indicated if the pain fails to respond to conservative measu ...[more]

PMID: 28580240

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Project description:Neuronal transmitters are released from nerve terminals via the fusion of synaptic vesicles with the plasma membrane. Vesicles attach to membranes via a specialized protein machinery composed of membrane-attached (t-SNARE) and vesicle-attached (v-SNARE) proteins that zipper together to form a coiled-coil SNARE bundle that brings the two fusing membranes into close proximity. Neurotransmitter release may occur either in response to an action potential or through spontaneous fusion. A cytosolic protein, Complexin (Cpx), binds the SNARE complex and restricts spontaneous exocytosis by acting as a fusion clamp. We previously proposed a model in which the interaction between Cpx and the v-SNARE serves as a spring to prevent premature zippering of the SNARE complex, thereby reducing the likelihood of fusion. To test this model, we combined molecular-dynamics (MD) simulations and site-directed mutagenesis of Cpx and SNAREs in Drosophila. MD simulations of the Drosophila Cpx-SNARE complex demonstrated that Cpx's interaction with the v-SNARE promotes unraveling of the v-SNARE off the core SNARE bundle. We investigated clamping properties in the syx3-69 paralytic mutant, which has a single-point mutation in the t-SNARE and displays enhanced spontaneous release. MD simulations demonstrated an altered interaction of Cpx with the SNARE bundle that hindered v-SNARE unraveling by Cpx, thus compromising clamping. We used our model to predict mutations that should enhance the ability of Cpx to prevent full assembly of the SNARE complex. MD simulations predicted that a weakened interaction between the Cpx accessory helix and the v-SNARE would enhance Cpx flexibility and thus promote separation of SNAREs, reducing spontaneous fusion. We generated transgenic Drosophila with mutations in Cpx and the v-SNARE that disrupted a salt bridge between these two proteins. As predicted, both lines demonstrated a selective inhibition in spontaneous release, suggesting that Cpx acts as a fusion clamp that restricts full SNARE zippering.

Dataset Information

Endoscopic Fusion of the Accessory Navicular Synchondrosis That Has No Diastasis.

Publications

Endoscopic Fusion of the Accessory Navicular Synchondrosis That Has No Diastasis.

Similar Datasets

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