Aim To determine the prevalence of glaucoma in patients with obstructive sleep apnoea. Design Cross-sectional case series. Participants One hundred patients with moderate to severe obstructive sleep apnoea.Testing Within 48 h of the polysomnographic diagnosis of obstructive sleep apnoea, patients underwent the following tests: intraocular pressure, gonioscopy, automated perimetry, stereoscopic biomicroscopy, and fundascopic assessment for the presence of glaucomatous optic nerve changes. Main outcome measures The prevalence of glaucoma in patients with obstructive sleep apnoea and the associations between patient characteristics and both glaucoma and intraocular pressure. Results Glaucoma was diagnosed in 27 of 100 patients yielding an estimated prevalence of 27% (95% CI 19-37%). The presence of glaucoma did not correlate with sex, body mass index (BMI), or AHI, but did appear to be associated with age (P ¼ 0.014). There was no evidence of a relationship between intraocular pressure and either the apnoea plus hypopnoea index or age. Conclusion The prevalence of glaucoma in patients with obstructive sleep apnoea is an estimated 27%. Sex, age, body mass index or apnoea plus hypopnoea index are not factors influencing the presence of glaucoma in this population of patients.

Common genetic alteration in cancer genomes is implicated for embracing an aberrant cancer gene participated in tumor progression. In this study, we identified a somatic mutated LIM and cysteine-rich domains-1 (LMCD1) as a putative metastatic oncogene in human hepatocellular carcinoma (HCC) using integrated genomic approaches. In addition to revealing genomic amplification and gene upregulation, we identified recurrent E135K (3/48 cases) mutations in HCC tissues and K237R mutation in the PLC/PRF/5 HCC cell line. Expression of mutant LMCD1 E135K or K237R reduced the stress fiber assembly, increased cortical actin accumulation and induced lamellipodial extension. Consistently, these mutations enhanced cell migration and showed activation of the Rac1-signaling pathway. Inhibition of the LMCD1/Rac1 pathway by an LMCD1 short-hairpin RNA (shLMCD1) or the Rac1 inhibitor NSC23766 suppressed the mutationmediated lamellipodial protrusion and cell migration. In PLC/PRF/5 cells with endogenous K237R mutation, cell migration was enhanced by estrogen-induced LMCD1 expression but reversed by shLMCD1 treatment. Moreover, overexpression of LMCD1 E135K mutation significantly promoted systemic lung metastasis in a murine tail vein injection model. Together, our results suggest that LMCD1 mutations are potential oncogenic events in HCC metastasis to promote cell migration through the Rac1-signaling pathway.

A novel method of protein array immobilization, using micro stamps to pick up proteins from micro wells and deposit them on to a bio-absorption chip, has been developed. This method can potentially transfer several protein spots on to an organized array for applications such as disease diagnosis and drug screening by parallel biological or chemical processes. Fabrication of the micro stamp and the micro well arrays involves thick-photoresist lithography, bulk micromachining, and a molding process, whereas fabrication of the bio-absorption chip involves amino-modification by use of APTS (aminopropyItrimethoxysilane) and surface activation by use of BS3 (bis-sulfosuccinimidyl suberate). Successful transfer of protein on to the bio-absorption surface using the micro stamp-well array has been demonstrated. The size variation between different stamping spots has been shown to be less than 10%, and the APTS-BS3 surface has also been proved to bind the protein efficiently. Appreciable protein retention was achieved during 6-h washing, which shows the binding strength of the bio-absorption surface is sufficient for protein processing.

Treatment with tibolone attenuated the development of OA, concomitantly reduced nociception and increased serum alkaline phosphatase in ACLT + OVX rats.