Unusual Cause of Acute Stroke in a Young Woman with Patent Foramen Ovale - Duplicated Inferior Vena Cava and May-Thurner Syndrome.

The etiology of acute ischemic stroke (AIS) may often remain uncertain despite diligent work-up, especially in young people. Although patent foramen ovale (PFO) is a frequent association during such work-up, the actual source of thromboembolism, like deep vein thrombosis (DVT), may not be found. Such associative pathology makes it challenging to prescribe anticoagulation for secondary stroke prevention.

Novel mechanism of increased Ca2+ release following oxidative stress in neuronal cells involves type 2 inositol-1,4,5-trisphosphate receptors.

Dysregulation of Ca(2+) signaling following oxidative stress is an important pathophysiological mechanism of many chronic neurodegenerative disorders, including Alzheimer's disease, age-related macular degeneration, glaucomatous and diabetic retinopathies. However, the underlying mechanisms of disturbed intracellular Ca(2+) signaling remain largely unknown. We here describe a novel mechanism for increased intracellular Ca(2+) release following oxidative stress in a neuronal cell line.

Inositol 1,4,5-triphosphate-associated cGMP kinase substrate: Basis Sequence: Mouse.

Inositol 1, 4, 5-trisphosphate (IP3) receptor associated cyclic GMP (cGMP) kinase substrate (IRAG, also known as Mrv1) is a type-2 integral membrane endoplasmic reticulum (ER) protein, which interacts with IP3 Receptor type 1 (IP3R1), cGMP kinase I-β (cGKI β) and other associated proteins. It plays a key role in NO, cGMP, and cGKI β mediated inhibition of IP3R1 activity and thus relaxes smooth muscle tone and inhibits platelet aggregation. As a scaffolding protein Mrv1 maintains the conformation of a heteroprotein complex containing cGKI β, IP3R1 and other proteins and enables efficient activity of cGKI β within the complex.