Acidic mammalian chitinase is not a critical target for allergic airway disease.

The expression of acidic mammalian chitinase (AMCase) is associated with Th2-driven respiratory disorders. To investigate the potentially pathological role of AMCase in allergic airway disease (AAD), we sensitized and challenged mice with ovalbumin or a combination of house dust mite (HDM) plus cockroach allergen. These mice were treated or not treated with small molecule inhibitors of AMCase, which significantly reduced allergen-induced chitinolytic activity in the airways, but exerted no apparent effect on pulmonary inflammation per se.

A role for endothelial selectins in allergic and nonallergic inflammatory disease.

Background: Several studies indicate that selectin-mediated leukocyte migration may depend on the types of initiating inflammatory stimuli or on the vascular beds involved in the inflammatory response. Thus, targeting selectin interactions to treat inflammation may have variable effects depending on the site and origin of the inflammatory response.

Objective: To address whether selectin-mediated leukocyte recruitment is stimulus or tissue dependent.

Three-dimensional sonography of the endometrium and adjacent myometrium: preliminary observations.

Objective: By evaluating a series of patients undergoing pelvic sonography with routine 2-dimensional (2D) as well as 3-dimensional (3D) reconstructed images in the coronal plane, we attempted to characterize the types of additional information that can be obtained.

Methods: Ninety randomly selected patients undergoing transvaginal pelvic sonography were imaged according to a standard 2D protocol. A 3D uterine volume was then acquired in the sagittal plane and reconstructed in the coronal plane.

Gob-5 contributes to goblet cell hyperplasia and modulates pulmonary tissue inflammation.

Gob-5 is a member of the calcium-activated chloride channel family and has been associated with allergic response in mouse models of pulmonary inflammation. Gene expression of Gob-5 has been shown to be induced in allergic airways and has been strongly associated with mucin gene regulation and goblet cell hyperplasia. We investigated the physiologic role of Gob-5 in murine models of pulmonary inflammation using mice deficient in Gob-5.