Recent advancements in embolic agents and endovascular techniques have led to increased interest in exploring endovascular embolization as a viable treatment for brain arteriovenous malformations. Several trials have investigated the use of various embolic agents for the treatment of arteriovenous malformations (AVMs) endovascularly. However, the reporting outcomes and design elements in these studies are heterogeneous and include inclusion/exclusion criteria and evaluated endpoints.
View Article and Find Full Text PDFAge-dependent formation of insoluble protein aggregates is a hallmark of many neurodegenerative diseases. We are interested in the cell chemistry that drives the aggregation of polyQ-expanded mutant Huntingtin (mHtt) protein into insoluble inclusion bodies (IBs). Using an inducible cell model of Huntington's disease, we show that a transient cold shock (CS) at 4 °C followed by recovery incubation at temperatures of 25-37 °C strongly and rapidly induces the compaction of diffuse polyQ-expanded Huntingtin-enhanced green fluorescent protein chimera protein (mHtt) into round, micron size, cytosolic IBs.
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