University of Udine

About: University of Udine is a education organization based out in Udine, Italy. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 6745 authors who have published 20530 publications receiving 669088 citations. The organization is also known as: Università degli Studi di Udine & Universita degli Studi di Udine.

Graphene-silicon phase modulators with gigahertz bandwidth

Abstract: The modulator is a key component in optical communications. Several graphene-based amplitude modulators have been reported based on electro-absorption. However, graphene phase modulators (GPMs) are necessary for functions such as applying complex modulation formats or making switches or phased arrays. Here, we present a 10 Gb s–1 GPM integrated in a Mach–Zehnder interferometer configuration. This is a compact device based on a graphene-insulator–silicon capacitor, with a phase-shifter length of 300 μm and extinction ratio of 35 dB. The GPM has a modulation efficiency of 0.28 V cm at 1,550 nm. It has 5 GHz electro-optical bandwidth and operates at 10 Gb s–1 with 2 V peak-to-peak driving voltage in a push–pull configuration for binary transmission of a non-return-to-zero data stream over 50 km of single-mode fibre. This device is the key building block for graphene-based integrated photonics, enabling compact and energy-efficient hybrid graphene–silicon modulators for telecom, datacom and other applications. A 10 Gb s–1 phase modulator based on a graphene-on-silicon Mach–Zehnder interferometer (MZI) is reported. The compact device has a phase-shifter length of only 300 μm and provides modulation of light at 1,550 nm with a 35 dB extinction ratio.

Efficacy and safety of belimumab in primary Sjögren's syndrome: results of the BELISS open-label phase II study

Abstract: Background Increased expression of B cell activating factor (BAFF or B lymphocyte stimulator) may explain the B cell activation characteristic of primary Sjogren9s syndrome (pSS). Objectives To evaluate the efficacy and safety of belimumab, targeting BAFF, in patients with pSS. Methods Patients were included in this bi-centric prospective 1-year open-label trial if they fulfilled American European Consensus group criteria, were anti-Sjogren9s syndrome A-positive and had current systemic complications or salivary gland enlargement, or early disease ( 25% improvement in any B cell activation biomarker values. Results Among 30 patients included, the primary end-point was achieved in 18 (60%). The mean (SD) European League Against Rheumatism (EULAR) Sjogren9s Syndrome Disease Activity Index decreased from 8.8 (7.4) to 6.3 (6.6) (p=0.0015) and EULAR) Sjogren9s Syndrome Patient Reported Index from 6.4 (1.1) to 5.6 (2.0) (p=0.0174). The mean dryness, fatigue and pain VAS varied from 7.8 (1.8) to 6.2 (2.9) (p=0.0021), 6.9 (1.8) to 6.0 (2.2) (p=0.0606) and 4.6 (2.6) to 4.7 (2.4) (p=0.89), respectively. Salivary flow and Schirmer9s test did not change. Conclusions These encouraging results justify future randomised controlled trials of belimumab in a selected target population of pSS patients most likely to benefit from treatment.

Disruptive mitochondrial DNA mutations in complex I subunits are markers of oncocytic phenotype in thyroid tumors

Abstract: Oncocytic tumors are a distinctive class of proliferative lesions composed of cells with a striking degree of mitochondrial hyperplasia that are particularly frequent in the thyroid gland. To understand whether specific mitochondrial DNA (mtDNA) mutations are associated with the accumulation of mitochondria, we sequenced the entire mtDNA in 50 oncocytic lesions (45 thyroid tumors of epithelial cell derivation and 5 mitochondrion-rich breast tumors) and 52 control cases (21 nononcocytic thyroid tumors, 15 breast carcinomas, and 16 gliomas) by using recently developed technology that allows specific and reliable amplification of the whole mtDNA with quick mutation scanning. Thirteen oncocytic lesions (26%) presented disruptive mutations (nonsense or frameshift), whereas only two samples (3.8%) presented such mutations in the nononcocytic control group. In one case with multiple thyroid nodules analyzed separately, a disruptive mutation was found in the only nodule with oncocytic features. In one of the five mitochondrion-rich breast tumors, a disruptive mutation was identified. All disruptive mutations were found in complex I subunit genes, and the association between these mutations and the oncocytic phenotype was statistically significant (P = 0.001). To study the pathogenicity of these mitochondrial mutations, primary cultures from oncocytic tumors and corresponding normal tissues were established. Electron microscopy and biochemical and molecular analyses showed that primary cultures derived from tumors bearing disruptive mutations failed to maintain the mutations and the oncocytic phenotype. We conclude that disruptive mutations in complex I subunits are markers of thyroid oncocytic tumors.