The use of magnetic nanowires is demonstrated as a new method for the application of force to mammalian cells. Magnetic separations were carried out on populations of NIH-3T3 mouse fibroblast cells using ferromagnetic Ni wires 350 nm in diameter and 35 microns long. Separation purities in excess of 90% and yields of 49% are obtained. The nanowires are shown to outperform magnetic beads of comparable volume.

Neuro-ophthalmological manifestations in moyamoya disease are usually the result of cerebrovascular involvement of the visual pathways. We report a case of ischemic optic neuropathy due to ocular hypoperfusion as a result of moyamoya disease, despite a prior internal to external carotid artery bypass with normal hemisphere perfusion. The blood supply of the optic nerve, a proposed pathogenesis of an anterior ischemic optic neuropathy and complications of the ocular ischemic syndrome are discussed.

SUMMARY:A 31-year-old woman with a prior history of Wyburn-Mason syndrome, complicated previously by a left thalamic intracerebral hemorrhage at age 21, complained of sudden left vision loss due to a central retinal vein occlusion. Angiography revealed a left thyroid arterio-venous malformation (AVM) in addition to ones found intracerebrally. The pathogenesis and embryogenesis of this finding including the management of AVMs in Wyburn-Mason syndrome are discussed. W yburn-Mason syndrome is an uncommon condition of brain-retinofacial angiomatosis resulting in multiple arteriovenous malformations (AVMs), usually on the ipsilateral side.1 Wyburn-Mason syndrome is now classified as a craniofacial arteriovenous metameric syndrome (CAMS).2 To date, thyroid AVMs with Wyburn-Mason syndrome have not been described. We describe a case of angiographically confirmed thyroid AVM in a clinically euthyroid patient with Wyburn-Mason syndrome. The embryology and possible pathogenesis, as well as management options for WyburnMason syndrome, are discussed. Case ReportA 31-year-old woman with Wyburn-Mason syndrome diagnosed at age 12 years with a known retinal AVM involving the left optic disc presented with sudden loss of vision in the left eye. Examination revealed a left central retinal vein occlusion with dilated tortuous retinal veins, optic disc swelling, and widespread retinal hemorrhages in all 4 quadrants. Her past history was significant for a left thalamic intracranial hemorrhage at age 21 years requiring a prolonged intensive care admission. She had no other neurologic symptoms.Formal 4-vessel cerebral digital subtraction angiography (DSA) was performed to evaluate the extent of her vascular malformations. It revealed a 3.0 ϫ 2.5-cm AVM in the left paramedian location along the medial aspect of the left internal carotid artery and optic tract, with an abnormal vascular blush within the left orbit and retina (Fig 1). The intracerebral AVM was fed by thalamic perforator arteries from the left posterior communicating artery (Fig 2), distal branches of the left internal carotid artery, anterior cerebral artery, and a prominent anterior choroidal artery. Incidentally, angiography also showed a left AVM of the thyroid gland (Fig 3), which is confirmed on multiple views and distinct from the laryngeal or paralaryngeal vessels. Her thyroid function tests were normal, and she has remained clinically euthyroid.Her central retinal vein occlusion was managed expectantly with regular review to monitor intraocular pressure and to observe for neovascularization. She has experienced no further hemorrhages from the AVMs in her eye, thyroid, or brain, nor has she had evidence of optic nerve compression.