Frequency Steerable Two Dimensional Focusing Using Rectilinear Leaky-Wave Lenses

The concept of frequency steerable two-dimensional electromagnetic focusing by using a tapered leaky-wave line source embedded in a parallel-plate medium is presented. Accurate expressions for analyzing the focusing pattern of a rectilinear leaky-wave lens (LWL) from its constituent leaky-mode tapered propagation constant are described. The influence of the main LWL structural parameters on the synthesis of the focusing pattern is discussed. The ability to generate frequency steerable focusing patterns has been demonstrated by means of an example involving a LWL in hybrid waveguide printed-circuit technology and the results are validated by a commercial full-wave solver.

Enhancing Frequency-Scanning Response of Leaky-Wave Antennas Using High-Impedance Surfaces

The use of high-impedance surfaces (HISs) to increase the frequency-scanning sensitivity of hollow leaky-wave antennas (LWAs) is presented. The LWA consists of a hollow rectangular waveguide with one of its narrow walls replaced by a partially reflective surface, and it is loaded with a metallodielectric HIS to increase its beam-scanning response. Theoretical results based on a simple transverse equivalent network illustrate the physical mechanism responsible for the improvement, and they are verified by experiments on a prototype working in the 11-16 GHz band.

1D-Leaky Wave Antenna Employing Parallel-Plate Waveguide Loaded With PRS and HIS

A new type of one-dimensional leaky-wave antenna (LWA) with independent control of the beam-pointing angle and beamwidth is presented. The antenna is based on a simple structure composed of a bulk parallel-plate waveguide (PPW) loaded with two printed circuit boards (PCBs), each one consisting of an array of printed dipoles. One PCB acts as a partially reflective surface (PRS), and the other grounded PCB behaves as a high impedance surface (HIS). It is shown that an independent control of the leaky-mode phase and leakage rate can be achieved by changing the lengths of the PRS and HIS dipoles, thus resulting in a flexible adjustment of the LWA pointing direction and directivity. The leaky-mode dispersion curves are obtained with a simple Transverse Equivalent Network (TEN), and they are validated with three-dimensional full-wave simulations. Experimental results on fabricated prototypes operating at 15 GHz are reported, demonstrating the versatile and independent control of the LWA performance by changing the PRS and HIS parameters.

Common variants at the MHC locus and at chromosome 16q24.1 predispose to Barrett's esophagus

Barrett's esophagus is an increasingly common disease that is strongly associated with reflux of stomach acid and usually a hiatus hernia, and it strongly predisposes to esophageal adenocarcinoma (EAC), a tumor with a very poor prognosis. We report the first genome-wide association study on Barrett's esophagus, comprising 1,852 UK cases and 5,172 UK controls in the discovery stage and 5,986 cases and 12,825 controls in the replication stage. Variants at two loci were associated with disease risk: chromosome 6p21, rs9257809 (P(combined) = 4.09 × 10(-9); odds ratio (OR) = 1.21, 95% confidence interval (CI) =1.13-1.28), within the major histocompatibility complex locus, and chromosome 16q24, rs9936833 (P(combined) = 2.74 × 10(-10); OR = 1.14, 95% CI = 1.10-1.19), for which the closest protein-coding gene is FOXF1, which is implicated in esophageal development and structure. We found evidence that many common variants of small effect contribute to genetic susceptibility to Barrett's esophagus and that SNP alleles predisposing to obesity also increase risk for Barrett's esophagus.

Abnormal changes in voltage-gated sodium channels NaV1.1, NaV1.2, NaV1.3, NaV1.6 and in Calmodulin/calmodulin-dependent protein kinase II, within the brains of spontaneously epileptic rats and tremor rats

Voltage-gated sodium channels (VGSCs) play a crucial role in epilepsy. The expressions of different VGSCs subtypes are varied in diverse animal models of epilepsy that may reflect their multiple phenotypes or the complexity of the mechanisms of epilepsy. In a previous study, we reported that NaV1.1 and NaV1.3 were up-regulated in the hippocampus of the spontaneously epileptic rat (SER). In this study, we further analyzed both the expression and distribution of the typical VGSC subtypes NaV1.1, NaV1.2, NaV1.3 and NaV1.6 in the hippocampus and in the cortex of the temporal lobe of two genetic epileptic animal models: the SER and the tremor rat (TRM). The expressions of calmodulin (CaM) and calmodulin-dependent protein kinase II (CaMKII) were also analyzed with the purpose of assessing the effect of the CaM/CaMKII pathway in these two models of epilepsy. Increased expression of the four VGSC subtypes and CaM, accompanied by a decrease in CaMKII was observed in the hippocampus of both the SERs and the TRM rats. However, the changes observed in the expression of VGSC subtypes and CaM were decreased with an elevated CaMKII in the cortex of their temporal lobes. Double-labeled immunofluorescence data suggested that in SERs and TRM rats, the four subtypes of the VGSC proteins were present throughout the CA1, CA3 and dentate gyrus regions of the hippocampus and temporal lobe cortex and these were co-localized in neurons with CaM. These data represent the first evidence of abnormal changes in expression of four VGSC subtypes (NaV1.1, NaV1.2, NaV1.3 and NaV1.6) and CaM/CaMKII in the hippocampus and temporal lobe cortex of SERs and TRM rats. These changes may be involved in the generation of epileptiform activity and underlie the observed seizure phenotype in these rat models of genetic epilepsy.

Sounds of the City

“Sounds of the City” is a large-scale community project and exhibition commissioned by the Metropolitan Arts Centre (MAC) and led by artists from the Sonic Arts Research Centre (SARC), Queen’s University Belfast. Over a four-month period, the artists worked together with two intergenerational groups in Belfast with the aim of addressing specific sound qualities of places, events and stories. Themes that surfaced from this process constitute the basis for the exhibition which promotes listening as a form of intersecting daily life, identity and memory. Five installations address aural contexts ranging from Belfast’s industrial heritage to the local family home. These are shaped by present and past experiences of workshop participants at Dee Street Community Centre in East Belfast and Tar Isteach in North Belfast. The themes and contents of these installations center upon the relationship between sound and memory, sound and place, and the documentation of everyday personal auditory experience.
All materials exhibited have emerged through workshops, interviews and field-recording sessions. Workshops acted as a basis from which to inform each group about the project’s aims, methods of listening, methods of documenting sound and the wider areas of soundscape studies and acoustic ecology. They also provided a central point allowing participants to organize outside activities and share material for exhibition.
“Sounds of the City” explores the relationship between sound and community through everyday life and presents a dynamic and ever-changing soundscape that shapes Belfast’s identity.

Sounds of the City has been exhibited at the MAC, Belfast 2012 and at Espaço Ecco, Brasilia 2013.

Next generation sequencing-based molecular diagnosis of retinitis pigmentosa: identification of a novel genotype-phenotype correlation and clinical refinements

Retinitis pigmentosa (RP) is a devastating form of retinal degeneration, with significant social and professional consequences. Molecular genetic information is invaluable for an accurate clinical diagnosis of RP due to its high genetic and clinical heterogeneity. Using a gene capture panel that covers 163 of the currently known retinal disease genes, including 48 RP genes, we performed a comprehensive molecular screening in a collection of 123 RP unsettled probands from a wide variety of ethnic backgrounds, including 113 unrelated simplex and 10 autosomal recessive RP (arRP) cases. As a result, 61 mutations were identified in 45 probands, including 38 novel pathogenic alleles. Interestingly, we observed that phenotype and genotype were not in full agreement in 21 probands. Among them, eight probands were clinically reassessed, resulting in refinement of clinical diagnoses for six of these patients. Finally, recessive mutations in CLN3 were identified in five retinal degeneration patients, including four RP probands and one cone-rod dystrophy patient, suggesting that CLN3 is a novel non-syndromic retinal disease gene. Collectively, our results underscore that, due to the high molecular and clinical heterogeneity of RP, comprehensive screening of all retinal disease genes is effective in identifying novel pathogenic mutations and provides an opportunity to discover new genotype-phenotype correlations. Information gained from this genetic screening will directly aid in patient diagnosis, prognosis, and treatment, as well as allowing appropriate family planning and counseling.

A genome-wide association study identifies new susceptibility loci for esophageal adenocarcinoma and Barrett's esophagus

Esophageal adenocarcinoma is a cancer with rising incidence and poor survival. Most such cancers arise in a specialized intestinal metaplastic epithelium, which is diagnostic of Barrett's esophagus. In a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individuals with precancerous Barrett's esophagus (n = 3,175) with 10,120 controls in 2 phases. For the combined case group, we identified three new associations. The first is at 19p13 (rs10419226: P = 3.6 × 10(-10)) in CRTC1 (encoding CREB-regulated transcription coactivator), whose aberrant activation has been associated with oncogenic activity. A second is at 9q22 (rs11789015: P = 1.0 × 10(-9)) in BARX1, which encodes a transcription factor important in esophageal specification. A third is at 3p14 (rs2687201: P = 5.5 × 10(-9)) near the transcription factor FOXP1, which regulates esophageal development. We also refine a previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 and extend our findings to now include esophageal adenocarcinoma.