Excessive production of airway mucus is a cardinal feature of bronchial asthma and chronic obstructive pulmonary disease (COPD) and contributes to morbidity and mortality in these diseases. IL-13, a Th2-type cytokine, is a central mediator in the pathogenesis of bronchial asthma, including mucus overproduction. Using a genome-wide search for genes induced in airway epithelial cells in response to IL-13, we identified pendrin encoded by the SLC26A4 (PDS) gene as a molecule responsible for airway mucus production. In both asthma and COPD mouse models, pendrin was up-regulated at the apical side of airway epithelial cells in association with mucus overproduction. Pendrin induced expression of MUC5AC, a major product of mucus in asthma and COPD, in airway epithelial cells. Finally, the enforced expression of pendrin in airway epithelial cells in vivo, using a Sendai virus vector, rapidly induced mucus overproduction in the lumens of the lungs together with neutrophilic infiltration in mice. These findings collectively suggest that pendrin can induce mucus production in airway epithelial cells and may be a therapeutic target candidate for bronchial asthma and COPD.

Trabeculectomy with MMC was less effective in maintaining intraocular pressure reduction in UG eyes than in POAG eyes. The prognostic factors for surgical failure of trabeculectomy in UG eyes were previous cataract surgery and granulomatous uveitis. In addition, UG eyes after trabeculectomy more frequently required additional cataract surgery.

The mouse Murr1 gene contains an imprinted gene, U2af1-rs1, in its first intron. U2af1-rs1 shows paternal allele-specific expression and is transcribed in the direction opposite to that of the Murr1 gene. In contrast to a previous report of biallelic expression of Murr1 in neonatal mice, we have found that the maternal allele is expressed predominantly in the adult brain and also preferentially in other adult tissues. This maternalpredominant expression is not observed in embryonic and neonatal brains. In situ hybridization experiments that used the adult brain indicated that Murr1 gene was maternally expressed in neuronal cells in all regions of the brain. We analyzed the developmental change in the expression levels of both Murr1 and U2af1-rs1 in the brain and liver, and we propose that the maternal-predominant expression of Murr1 results from transcriptional interference of the gene by U2af1-rs1 through the Murr1 promoter region.

Trabeculectomy with mitomycin C may be more effective than viscocanalostomy in lowering intraocular pressure in patients with primary open-angle glaucoma, while eyes undergoing viscocanalostomy experience a lower incidence of complications. Further investigation of more cases is needed.

Aim: To study a correlation between age at the onset and myopic refraction and axial length in patients with idiopathic macular hole and to evaluate a correlation of the size and surgical outcome of macular hole with axial length. Methods: In a prospective clinical study, 94 eyes of 91 patients with stage III and IV idiopathic macular hole were enrolled. A standardised surgical protocol was performed using vitrectomy and gas tamponade. This study evaluated the size of macular hole and the rate of anatomical and functional success of surgery. To assess dimensions of macular hole, confocal laser scanning tomography was employed.Results: Age at the onset showed a significant increase in relation to myopic refraction and axial length (r = 0.689, p <0.0001; r = 0.723, p <0.0001). Mean age was 52. I n the age related macular holes, vitreoretinal surgical techniques have been used to close macular holes based on theory that the tangentially oriented contraction of the premacular vitreous cortex is involved in the pathogenesis of macular holes.1-3 The procedure for repairing a macular hole involves the removal of the premacular cortical vitreous and the performance of intraocular gas tamponade. Theories regarding the mechanisms by which closure of macular hole occurs include the release of vitreous traction and the formation of a glial scar. [1][2][3][4][5][6][7][8][9][10] Highly myopic individuals are known to be a high risk group for macular holes. The early stages of age related macular holes have been described, 1-10 but it is uncertain whether the degree of myopic refraction may influence the development of macular hole. 12The objective of the present study was to study the effect of myopic refraction on the development of macular hole. We also investigated a relation between refractive error and the size of macular hole, and anatomical and visual improvement of surgery. MATERIALS AND METHODS PatientsWe studied 94 eyes of 91 Japanese patients with idiopathic full thickness stage III and IV macular holes who had symptoms present for 6 months or shorter and were scheduled to undergo macular hole surgery. Any patient with pre-existing ocular disease (that is, trauma, chronic inflammatory, or neoplastic disorders) or previous surgery were excluded as were those with systemic disorders (diabetes, uncontrolled hypertension) or a known life threatening disease at enrolment into the study. Patients were informed of the purpose of our study and provided written informed consent. Macular holes were diagnosed based on the results of slit lamp biomicroscopy with a precorneal lens, indirect ophthalmoscopy, and fluorescein angiography. A macular hole was defined as a full thickness, sharp-edged retinal defect with an elevated rim and retinal striae in the foveal area with a hyperfluorescent window defect visible on fluorescein angiography.