Evaluation of a revised indication for determining adult cochlear implant candidacy.

Objective: To evaluate the use of monosyllabic word recognition versus sentence recognition to determine candidacy and long-term benefit for cochlear implantation.

Study Design: Prospective multi-center single-subject design.

Methods: A total of 21 adults aged 18 years and older with bilateral moderate to profound sensorineural hearing loss and low monosyllabic word scores received unilateral cochlear implantation.

MicroRNA expression profile in human macrophages in response to Leishmania major infection.

Background: Leishmania (L.) are intracellular protozoan parasites able to survive and replicate in the hostile phagolysosomal environment of infected macrophages. They cause leishmaniasis, a heterogeneous group of worldwide-distributed affections, representing a paradigm of neglected diseases that are mainly embedded in impoverished populations.

Objective findings with malpositioning of a nucleus 24RE(CA) cochlear implant.

Background: Proper intracochlear placement of cochlear implant electrode arrays is believed to be important for optimum speech perception results. However, objective tests of cochlear implant function typically provide little or no information about the intracochlear placement of the array. We report the results for a variety of objective tests, including averaged electrode voltage (AEV) measurements, in a patient where the electrode array had folded up on itself during insertion.

LPA modulates monocyte migration directly and via LPA-stimulated endothelial cells.

Lysophosphatidic acid (LPA) is a bioactive lysophospholipid ligand present in oxidized low-density lipoprotein. The effects of LPA were investigated, first separately on endothelial cells (EC) and monocytes. Using Ki16425 (an LPA(1) and LPA(3) receptor antagonist), GW9662 [a peroxisome proliferator-activator receptor (PPARgamma) antagonist], and pertussis toxin (that inhibits G(i/o)), we demonstrate that LPA enhances IL-8 and monocyte chemoattractant protein-1 expression through a LPA(1)-, LPA(3)-, G(i/o)- and PPARgamma-dependent manner in the EAhy926 cells.

Upregulation of pentraxin-3 in human endothelial cells after lysophosphatidic acid exposure.

Objective: The earliest event in atherogenesis appears to be endothelium dysfunction. Lysophosphatidic acid (LPA), one of the major bioactive lipid components of oxidized low-density lipoproteins (oxLDL), can cause the activation of endothelial cells (ECs), which start to secrete multiple proinflammatory polypeptides/proteins. The purpose of this study was to better document the proatherogenic properties of LPA using a subproteomic approach focused on the secretome of LPA-treated ECs.