Compact Bandwidth Enhanced Cavity-Backed Magneto-Electric Dipole Antenna with Outer Γ-Shaped Probe for GNSS Bands.

In this paper, a wideband small cavity-backed magneto-electric (ME) antenna is proposed. This antenna is linearly polarized and designed to cover all the Global Navigation Satellite System (GNSS) bands. It exhibits small external dimensions of 90 × 90 × 40 mm3 (0.34 × 0.34 × 0.15 λ3 at lowest frequency) and achieves a wide impedance bandwidth of 40.5% (from 1.14 to 1.72 GHz) due to the excitation of a third resonance of the ME structure. It also provides a regular broadside gain of 5.2 dBi and stable radiation pattern in both E and H planes of the antenna.

Prevalence of Unknown Ocular Hypertension, Glaucoma Suspects, and Glaucoma in Patients Seen in an Ophthalmology Center in France.

INTRODUCTION: The rate of unknown glaucoma is around 50% in industrialized countries. The purpose of our study was to estimate the prevalence of unknown cases of ocular hypertension, glaucoma suspects, and glaucoma in patients consulting for refractive disorders in France. METHODS: A retrospective study in the Point Vision ophthalmology center was led in Toulouse, France. All participants consulting for refractive disorders between June 2015 and June 2017 in the ophthalmology center were included. The cases were identified by the assessment of intraocular pressure, optic nerve head structure, and visual field. Ocular hypertension was defined as an intraocular pressure >21 mm Hg. Glaucoma was defined as the association of a glaucomatous papilla and two successive pathological visual fields. Glaucoma suspect was defined as the association of a glaucomatous papilla without visual field defect. The primary endpoint was the prevalence of unknown ocular hypertension, glaucoma suspects, and glaucoma in patients seen in an ophthalmology center. RESULTS: A total of 66,068 patients (mean age = 37 years) consulted for a refraction visual assessment during the study period. Among them, 234 had a visual field and a retinal nerve fiber layer assessment for ocular hypertension and/or suspicious papilla. The prevalence of unknown cases of ocular hypertension, glaucoma suspect, and glaucoma was 2.6, 0.8, and 0.5 per 1,000 consultants, respectively. Median age at diagnosis of ocular hypertension, glaucoma suspect, and glaucoma was 52, 53, and 65 years, respectively. CONCLUSION: The present study highlights the importance of glaucoma screening in people over 40 years old with the measurement of intraocular pressure and an optic nerve head assessment.

Targeted resequencing identifies PTCH1 as a major contributor to ocular developmental anomalies and extends the SOX2 regulatory network.

Ocular developmental anomalies (ODA) such as anophthalmia/microphthalmia (AM) or anterior segment dysgenesis (ASD) have an estimated combined prevalence of 3.7 in 10,000 births. Mutations in SOX2 are the most frequent contributors to severe ODA, yet account for a minority of the genetic drivers. To identify novel ODA loci, we conducted targeted high-throughput sequencing of 407 candidate genes in an initial cohort of 22 sporadic ODA patients. Patched 1 (PTCH1), an inhibitor of sonic hedgehog (SHH) signaling, harbored an enrichment of rare heterozygous variants in comparison to either controls, or to the other candidate genes (four missense and one frameshift); targeted resequencing of PTCH1 in a second cohort of 48 ODA patients identified two additional rare nonsynonymous changes. Using multiple transient models and a CRISPR/Cas9-generated mutant, we show physiologically relevant phenotypes altering SHH signaling and eye development upon abrogation of ptch1 in zebrafish for which in vivo complementation assays using these models showed that all six patient missense mutations affect SHH signaling. Finally, through transcriptomic and ChIP analyses, we show that SOX2 binds to an intronic domain of the PTCH1 locus to regulate PTCH1 expression, findings that were validated both in vitro and in vivo. Together, these results demonstrate that PTCH1 mutations contribute to as much as 10% of ODA, identify the SHH signaling pathway as a novel effector of SOX2 activity during human ocular development, and indicate that ODA is likely the result of overactive SHH signaling in humans harboring mutations in either PTCH1 or SOX2.