One-stage coclear implantation via a facial recess approach in children with otitis media with effusion

AbstractObjectiveTo investigate surgical indications, operative techniques, complications and auditory and speech rehabilitation for cochlear implant (CI) in children with otitis media with effusion (OME).Material and methodsThis is a retrospective review of records of 24children with bilateral profound sensorineural hearing loss and OME who were implanted during January 2011 to November 2014 in the Department of Otorhinolaryngology and Head and Neck Surgery at the PLA Hospital, using one-stage implantation via the facial recess approach and round window insertion. The incus was removed in 8 cases during the implantation procedure. Local infiltration of dexamethasone and adrenaline in the middle ear was also performed. Postoperative complications were examined. Preoperative and postoperative questionnaires including Categories of Auditory Performance (CAP), Speech Intelligibility Rating (SIR), and the Meaningful Auditory Integration Scale (MAIS) were collected.ResultsAll electrodes were implanted successfully without any immediate or delayed complications. Inflammatory changes of middle ear mucosa with effusion were noted in all implanted ears. The scores of post-implant CAP and SIR increased significantly in all 24 cases (t = −25.95 and −14.09, respectively for CAP and SIR, p < 0.05).ConclusionsOne-stage CI via the facial recess approach with round window insertion is safe and effective in cochlear implant candidates with OME, as seen in the 24 children in our study who achieved improved auditory performance and speech intelligibility after CI

4-Acetyl-2,3,4,5-tetra­hydro-1H-1,4-benzodiazepine

The title compound, C11H14N2O·H2O, crystallizes with one formula unit in the asymmetric unit. The seven-membered ring has a chair conformation with the C=O group turned away from the benzene ring. N—H⋯O and O—H⋯O hydrogen bonds are present in the crystal structure

catena-Poly[[diaquacadmium(II)]bis­(μ-pyridine-3-sulfonato)-κ2 N:O;κ2 O:N]

In the title polymeric complex, [Cd(C5H4NO3S)2(H2O)2]n, the Cd atom is located on a centre of inversion and is coordinated by two O atoms and two N atoms, derived from four different pyridine-3-sulfonate ligands, and two O atoms derived from two water mol­ecules, forming a distorted trans-N2O4 octa­hedral geometry. The topology of the polymer is a one-dimensional chain mediated by bridging pyridine-3-sulfonate anions. These are connected into a three-dimensional architecture via hydrogen bonds

ER-α36, a Novel Variant of ER-α, Mediates Estrogen-Stimulated Proliferation of Endometrial Carcinoma Cells via the PKCδ/ERK Pathway

Recently, a variant of ER-α, ER-α36 was identified and cloned. ER-α36 lacks intrinsic transcription activity and mainly mediates non-genomic estrogen signaling. The purpose of this study was to investigate the function and the underlying mechanisms of ER-α36 in growth regulation of endometrial Ishikawa cancer cells.The cellular localization of ER-α36 and ER-α66 were determined by immunofluorescence in the Ishikawa cells. Ishikawa endometrial cancer control cells transfected with an empty expression vector, Ishikawa cells with shRNA knockdown of ER-α36 (Ishikawa/RNAiER36) and Ishikawa cells with shRNA knockdown of ER-α66 (Ishikawa/RNAiER66) were treated with E2 and E2-conjugated to bovine serum albumin (E2-BSA, membrane impermeable) in the absence and presence of different kinase inhibitors HBDDE, bisindolylmaleimide, rottlerin, H89 and U0126. The phosphorylation levels of signaling molecules and cyclin D1/cdk4 expression were examined with Western blot analysis and cell growth was monitored with the MTT assay.Immunofluorescence staining of Ishikawa cells demonstrated that ER-α36 was expressed mainly on the plasma membrane and in the cytoplasm, while ER-α66 was predominantly localized in the cell nucleus. Both E2 and E2-BSA rapidly activated PKCδ not PKCα in Ishikawa cells, which could be abrogated by ER-α36 shRNA expression. E2-and E2-BSA-induced ERK phosphorylation required ER-α36 and PKCδ. However, only E2 was able to induce Camp-dependent protein kinase A (PKA) phosphorylation. Furthermore, E2 enhances cyclin D1/cdk4 expression via ER-α36.E2 activates the PKCδ/ERK pathway and enhances cyclin D1/cdk4 expression via the membrane-initiated signaling pathways mediated by ER-α36, suggesting a possible involvement of ER-α36 in E2-dependent growth-promoting effects in endometrial cancer cells