Purpose To analyse nocturnal intraocular pressure (IOP) fluctuations in patients with obstructive sleep apnea syndrome (OSAS) using a contact lens sensor (CLS) and to identify associations between the OSAS parameters determined by polysomnographic study (PSG) and IOP changes. Method Prospective, observational study. Twenty participants suspected of having OSAS were recruited. During PSG study, IOP was monitored using a CLS placed in the eye of the patient. The patients were classified according to the apnea-hypopnea index (AHI) in two categories, severe (> 30) or mild/moderate (< 30) OSAS. We evaluated several parameters determined by the IOP curves, including nocturnal elevations (acrophase) and plateau times in acrophase (PTs) defined by mathematical and visual methods. Results The IOP curves exhibited a nocturnal acrophase followed by PTs of varying extents at which the IOP remained higher than daytime measurement with small variations. We found significant differences in the length of the PTs in patients with severe OSAS compared to those with mild/moderate disease (P = 0.032/P = 0.028). We found a positive correlation between PTs and OSAS severity measured by the total number of apneic events (r = 0.681/ 0.751 P = 0.004/0.001) and AHI (r = 0.674/0.710, P = 0.004/0.002). Respiratory-related arousal and oxygen saturation also were associated significantly with the IOP PT length. Conclusions Periods of nocturnal IOP elevation lasted longer in severe OSAS patients than those with mild/moderate OSAS and correlate with the severity of the disease. The length of the nocturnal PT is also associated to respiratory parameters altered in patients with OSAS.

BackgroundTear film stability is the key event in ocular surface diseases. The purpose of this study is to evaluate spatial and temporal progression of the tear film breakup using an automatic non-invasive device.MethodsNon-invasive tear breakup time (NITBUT) parameters, such as First NITBUT (F-NITBUT) and Average NITBUT (A-NITBUT), were evaluated in 132 glaucoma and 87 control eyes with the Keratograph 5M device. Further analysis of this data was used to determine size, location and progression of tear film breakup with automatically identified breakup areas (BUA). The progression from First BUA (F-BUA) to total BUA (T-BUA) was expressed as Dry Area Growth Rate (DAGR). Differences between both groups were analysed using Student t-test for parametric data and Mann-Whitney U test for non-parametric data. Pearson's correlation coefficient was used to assess the relationship between parametric variables and Spearman in the case of non-parametric variables.ResultsF-NITBUT was 11.437.83s in the control group and 8.17 +/- 5.73 in the glaucoma group (P=0.010). A-NITBUT was 14.04 +/- 7.21 and 11.82 +/- 6.09s in control and glaucoma groups, respectively (P=0.028). F-BUA was higher in the glaucoma group than in the control group (2.73 and 2.28; P=0.022) and was more frequently located at the centre of the cornea in the glaucoma group (P=0.039). T-BUA was also higher in the glaucoma group than in the control group (13.24 and 9.76%; P=0.012) and the DAGR was steeper in the glaucoma group than in the control group (34.38 degrees and 27.15 degrees; P=0.009).Conclusions Shorter NITBUT values and bigger, more central tear film breakup locations were observed in the glaucoma group than in the control group. The DAGR indicates that tear film rupture is bigger and increases faster in glaucomatous eyes than in normal eyes.

Purpose To evaluate the quality of life of glaucoma patients using the Ocular Surface Disease Index (OSDI) questionnaire and their association with dry eye clinical signs. Methods The study included patients into three groups. The treated group diagnosed with bilateral open-angle glaucoma and treated with one or more topical medication at least 1 year. The operated group underwent glaucoma surgery without the need for topical medications. The control group entered subjects without ocular diseases or previous surgeries. Dry eye clinical signs were evaluated; noninvasive tear break-up time, Meibomian gland depletion (MGD), and conjunctival hyperemia were measured using the Keratograph 5 M. The total-OSDI (T-OSDI) score was divided into the visual field-OSDI and discomfort-OSDI scores. Results Two hundred and nine subjects participated in this cross-sectional study, 147 using glaucoma medications, 21 patients underwent glaucoma surgery and 41 were controls. The T-OSDI and subscores were higher in glaucoma patients compared with controls (p < 0.05); we found no differences between treated and surgically groups. Correlations were observed between the T-OSDI values and Schirmer test (p = 0.016), ocular surface staining (p < 0.001) and the MGD (p = 0.006). The subscores were associated with the ocular surface staining (VF p = 0.013 and D p = 0.003). In treated patients, the number of drops per day correlates with T-OSDI and subscores (p = 0.017 and p = 0.005). Conclusion OSDI scores increased in the glaucoma patients compared to controls without significant changes between treated and surgical patients. OSDI scores were associated to dry eye signs and medication in glaucoma patients.

Long non-coding RNAs (lncRNAs) play critical roles in diverse cellular processes; however, their involvement in many critical aspects of the immune response including the interferon (IFN) response remains poorly understood. To address this gap, we compared the global gene expression pattern of primary human hepatocytes before and at three time points after treatment with IFN-¿. Among ~ 200 IFN-induced lncRNAs, one transcript showed ~ 100-fold induction. This RNA, which we named lncRNA-CMPK2, was a spliced, polyadenylated nuclear transcript that was induced by IFN in diverse cell types from human and mouse. Similar to protein-coding IFN-stimulated genes (ISGs), its induction was dependent on JAK-STAT signaling. Intriguingly, knockdown of lncRNA-CMPK2 resulted in a marked reduction in HCV replication in IFN-stimulated hepatocytes, suggesting that it could affect the antiviral role of IFN. We could show that lncRNA-CMPK2 knockdown resulted in upregulation of several protein-coding antiviral ISGs. The observed upregulation was caused by an increase in both basal and IFN-stimulated transcription, consistent with loss of transcriptional inhibition in knockdown cells. These results indicate that the IFN response involves a lncRNA-mediated negative regulatory mechanism. lncRNA-CMPK2 was strongly upregulated in a subset of HCV-infected human livers, suggesting a role in modulation of the IFN response in vivo.

The hepatitis C virus (HCV) was discovered by the team of Michael Houghton at Chiron Corporation in 1989 and the first symposium on HCV and related viruses was held in Venice, Italy, shortly after, in 1992. This conference was organized to advance knowledge on what then was a mysterious virus responsible for most cases of «non-A, non-B» hepatitis. During the 20 years since the first conference, the scientific quality of presentations has steadily increased, together with the tremendous advances in basic and clinical research and epidemiology. What started as a small conference on a new virus, about which there were very few data, has today become a first-in-class congress: a meeting place for basic researchers, clinicians, epidemiologists, public health experts, and industry members to present the most important advances and their application to HCV treatment and control. The nineteenth HCV symposium was held in September 2012, once again in Venice.

La primera conferencia sobre el virus de la hepatitis C (VHC) y otros virus relacionados se celebró en Venecia en 1992, poco después de su descubrimiento en 1989 por el equipo de Michael Houghton en la Chiron Corporation. Esta conferencia se planteó con el objetivo de avanzar en los conocimientos sobre el entonces misterioso virus responsable de la mayoría de las hepatitis «no A, no B». Durante estos 20 años desde la primera conferencia, su nivel científico ha ido incrementándose proporcionalmente a los avances en la investigación básica, epidemiológica y clínica. Lo que comenzó siendo un pequeño simposio sobre un nuevo virus del que se conocía bien poco, se ha convertido en el congreso de referencia: un punto de encuentro de investigadores básicos, clínicos, epidemiólogos y expertos en salud pública, y miembros de la industria donde se presentan los avances más importantes y su aplicación al tratamiento y control de la infección. El pasado mes de septiembre de 2012 se celebró la decimonovena edición, de nuevo en Venecia.

Adenovirus infection has a tremendous impact on the cellular silencing machinery. Adenoviruses express high amounts of non-coding virus associated (VA) RNAs able to saturate key factors of the RNA interference (RNAi) processing pathway, such as Exportin 5 and Dicer. Furthermore, a proportion of VA RNAs is cleaved by Dicer into viral microRNAs (mivaRNAs) that can saturate Argonaute, an essential protein for miRNA function. Thus, processing and function of cellular miRNAs is blocked in adenoviral-infected cells. However, viral miRNAs actively target the expression of cellular genes involved in relevant functions such as cell proliferation, DNA repair or RNA regulation. Interestingly, the cellular silencing machinery is active at early times post-infection and can be used to control the adenovirus cell cycle. This is relevant for therapeutic purposes against adenoviral infections or when recombinant adenoviruses are used as vectors for gene therapy. Manipulation of the viral genome allows the use of adenoviral vectors to express therapeutic miRNAs or to be silenced by the RNAi machinery leading to safer vectors with a specific tropism. This article is part of a "Special Issue entitled:MicroRNAs in viral gene regulation".