Larynx: anatomic imaging for diagnosis and management.

Imaging with CT, MRI, or fluorodeoxyglucose F 18-positron emission tomography is often an important complement to laryngoscopy for diagnosis and management of laryngeal pathology. At most centers, CT is the most popular modality for general laryngeal imaging given its widespread availability, ease of acquisition, and familiarity to clinicians, whereas MRI and positron emission tomography are used as problem-solving tools. Frequent indications for laryngeal imaging include cancer staging, suspected submucosal abnormalities, vocal cord paralysis, laryngeal trauma, and laryngotracheal stenosis. This article reviews the primary imaging modalities used for evaluation of, normal cross-sectional anatomy of, and radiologic features of common diseases of the larynx.

De novo cerebral arteriovenous malformation in a child with previous cavernous malformation and developmental venous anomaly.

Although cerebral vascular malformations are traditionally considered to be congenital lesions, they often become clinically evident in the 3rd to 4th decades of life, leading to the assumption of a long silent clinical period. Unlike vein of Galen malformations, antenatal diagnosis of cerebral arteriovenous malformations (AVMs) is highly uncommon. Postnatal development of an AVM is an emergent concept supported by more clinical observations. Genetic and biological studies demonstrate that an environmental trigger ("second hit") in addition to genetic predisposition may be a key in understanding the pathophysiology of AVMs and other cerebral vascular lesions such as cavernous malformations (CMs). The authors describe a 6-year-old boy in whom a giant CM was diagnosed and a de novo AVM was detected 25 months after initial resection of the CM. This case seems to support the second-hit hypothesis.

Receptors and signaling mechanisms required for prostaglandin E2-mediated regulation of mast cell degranulation and IL-6 production.

Mast cells are implicated in the pathogenesis of a broad spectrum of immunological disorders. These cells release inflammatory mediators in response to a number of stimuli, including IgE-Ag complexes. The degranulation of mast cells is modified by PGs. To begin to delineate the pathway(s) used by PGs to regulate mast cell function, we examined bone marrow-derived mast cells (BMMC) cultured from mice deficient in the EP(1), EP(2), EP(3), and EP(4) receptors for PGE(2). Although BMMCs express all four of these PGE(2) receptors, potentiation of Ag-stimulated degranulation and IL-6 cytokine production by PGE(2) is dependent on the EP(3) receptor. Consistent with the coupling of this receptor to G(alphai), PGE(2) activation of the EP(3) receptor leads to both inhibition of adenylate cyclase and increased intracellular Ca(2+). The magnitude of increase in intracellular Ca(2+) induced by EP(3) activation is similar to that observed after activation of cells with IgE and Ag. Although PGE alone is not sufficient to initiate BMMC degranulation, stimulation of cells with PGE along with PMA induces degranulation. These actions are mediated by the EP(3) receptor through signals involving Ca(2+) mobilization and/or decreased cAMP levels. Accordingly, these studies identify PGE(2)/EP(3) as a proinflammatory signaling pathway that promotes mast cell activation.