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“Background: Olfaction has been demonstrated to have a great impact on patients’ lives. Transsphenoidal endoscopic pituitary surgery is associated with potentially significant damage to olfactory tissues, but to date this issue has been only poorly documented in the literature.\n\nStudy Design: Prospective cohort study comparing olfactory outcomes pre- and postpituitary surgery.\n\nMethod: Patients were administered the University of Pennsylvania Smell Identification Test (UPSIT) preoperatively and again at 6 months postoperatively. The endoscopic transsphenoidal pituitary surgery was carried out using a full middle

turbinate MEK inhibitor preservation protocol. A Hadad-Bassagasteguy (HB) vascularized septal flap was raised in each case. Secondary outcomes included Lund-Kennedy endoscopy scores (LKES) and patient self-report of olfactory disturbance.

The results were analysed using a paired t-tests.\n\nResults: Seventeen patients met inclusion criteria for the study. Mean preoperative UPSIT value was 37.2 (normosmia), and mean postoperative UPSIT value was 30.8 (moderate hyposmia) (P < .001). All patients were fully healed with normal LKES scores by 6 months. All patients complained of their olfactory dysfunction.\n\nConclusions: learn more This study is the first to describe postoperative olfactory perturbations suffered by patients undergoing endoscopic transsphenoidal pituitary surgery. We hypothesize that olfactory impairment results from use of the HB flap. We recommend that the possibility of permanent olfactory changes be added to routine patient counseling and consent for this procedure, and that HB flaps be raised judiciously during trannssphenoidal endoscopic procedures.”
“Background: Eosinophils are important effector cells in the pathogenesis of allergic diseases such as bronchial asthma. Oxidative stress in the form of cellular reactive oxygen species (ROS) has been implicated in the

pathogenesis of several allergic diseases. Recently, it has become evident that mitochondrial-derived ROS are important transducers of apoptosis and intracellular signaling. In this study, we investigated the LXH254 role of mitochondrial ROS in the activation of extracellular signal-regulated kinases (ERK) 1 and 2-mitogen-activated protein kinase (MAPK) and caspase-3 in human eosinophils stimulated with H(2)O(2).\n\nMethods: Human eosinophils were purified using immunomagnetic negative selection and then stimulated with H(2)O(2), H(2)O(2)-induced eosinophil apoptosis was measured by staining cells with annexin V. Activation of ERK1/2 MAPK and caspases was assessed by Western blotting. Eosinophils were pretreated with rotenone, an inhibitor of the mitochondrial electron transport chain, before H(2)O(2) was added.\n\nResults: Treatment with 1 mM H(2)O(2) induced externalization of phosphatidylserine (PS) and activation of caspases in eosinophils.