Influence of hydrogen on paramagnetic defects induced by UV laser exposure in natural silica

Diffusion limited reactions of point defects were investigated in amorphous SiO2 exposed to UV laser light. Electron spin resonance and in situ absorption measurements at room temperature evidenced the annealing of E' centers and the growth of H(II) centers both occurring in the post-irradiation stage and lasting a few hours. These transients are caused by reactions involving molecular hydrogen H2, made available by dimerization of radiolytic H0.Comment: Submitted to Physica Status Solid

Photoluminescence dispersion as a probe of structural inhomogeneity in silica

We report time-resolved photoluminescence spectra of point defects in amorphous silicon dioxide (silica), in particular the decay kinetics of the emission signals of extrinsic Oxygen Deficient Centres of the second type from singlet and directly-excited triplet states are measured and used as a probe of structural inhomogeneity. Luminescence activity in sapphire ($\alpha$-Al$_2$O$_3$) is studied as well and used as a model system to compare the optical properties of defects in silica with those of defects embedded in a crystalline matrix. Only for defects in silica, we observe a variation of the decay lifetimes with emission energy and a time dependence of the first moment of the emission bands. These features are analyzed within a theoretical model with explicit hypothesis about the effect introduced by the disorder of vitreous systems. Separate estimations of the homogenous and inhomogeneous contributions to the measured emission linewidth are obtained: it is found that inhomogeneous effects strongly condition both the triplet and singlet luminescence activities of oxygen deficient centres in silica, although the degree of inhomogeneity of the triplet emission turns out to be lower than that of the singlet emission. Inhomogeneous effects appear to be negligible in sapphire

H(II) centers in natural silica under repeated UV laser irradiations

We investigated the kinetics of H(II) centers (=Ge'-H) in natural silica under repeated 266nm UV irradiations performed by a Nd:YAG pulsed laser. UV photons temporarily destroy these paramagnetic defects, their reduction being complete within 250 pulses. After re-irradiation, H(II) centers grow again, and the observed recovery kinetics depends on the irradiation dose; multiple 2000 pulses re-irradiations induce the same post-irradiation kinetics of H(II) centers after each exposure cycle. The analysis of these effects allows us to achieve a deeper understanding of the dynamics of the centers during and after laser irradiation.Comment: Submitted to Journal of Non Crystalline Solid

Optical properties of Ge-oxygen defect center embedded in silica films

The photo-luminescence features of Ge-oxygen defect centers in a 100nm thick Ge-doped silica film on a pure silica substrate were investigated by looking at the emission spectra and time decay detected under synchrotron radiation excitation in the 10-300 K temperature range. This center exhibits two luminescence bands centered at 4.3eV and 3.2eV associated with its de-excitation from singlet (S1) and triplet (T1) states, respectively, that are linked by an intersystem crossing process. The comparison with results obtained from a bulk Ge-doped silica sample evidences that the efficiency of the intersystem crossing rate depends on the properties of the matrix embedding the Ge-oxygen defect centers, being more effective in the film than in the bulk counterpart.Comment: 10 pages, 3 figures, in press on J. Non cryst. solids (2007

Influence of fluorine on the fiber performance studied through the NBOHC-related 1.9 eV microluminescence

The distribution of Non Bridging Oxygen Hole Centers (NBOHC) in Fluorine doped optical fibers was investigated by confocal microluminescence spectroscopy monitoring the characteristic 1.9 eV luminescence band. The results show that these defects are generated by the fiber drawing and their concentration further increases after \u3b3 irradiation. The NBOHC profile along the fiber is anticorrelated to the fluorine content. This finding agrees with the role of fluorine in the fiber toughness and is discussed from the microscopic point of view on the basis of previous works

Radiation hardening techniques for rare-earth based optical fibers and amplifiers

Er/Yb doped fibers and amplifiers have been shown to be very radiation sensitive, limiting their integration in space. We present an approach including successive hardening techniques to enhance their radiation tolerance. The efficiency of our approach is demonstrated by comparing the radiation responses of optical amplifiers made with same lengths of different rare-earth doped fibers and exposed to gamma-rays. Previous studies indicated that such amplifiers suffered significant degradation for doses exceeding 10 krad. Applying our techniques significantly enhances the amplifier radiation resistance, resulting in a very limited degradation up to 50 krad. Our optimization techniques concern the fiber composition, some possible pre-treatments and the interest of simulation tools used to harden by design the amplifiers. We showed that adding cerium inside the fiber phosphosilicate-based core strongly decreases the fiber radiation sensitivity compared to the standard fiber. For both fibers, a pre-treatment with hydrogen permits to enhance again the fiber resistance. Furthermore, simulations tools can also be used to improve the tolerance of the fiber amplifier by helping identifying the best amplifier configuration for operation in the radiative environment

Structural relaxation of E' gamma centers in amorphous silica

We report experimental evidence of the existence of two variants of the E' gamma centers induced in silica by gamma rays at room temperature. The two variants are distinguishable by the fine features of their line shapes in paramagnetic resonance spectra. These features suggest that the two E' gamma differ for their topology. We find a thermally induced interconversion between the centers with an activation energy of about 34 meV. Hints are also found for the existence of a structural configuration of minimum energy and of a metastable state.Comment: 4 pages, 2 figures, submitted to Phys. Rev. Let

Duchenne's muscular dystrophy involves a defective transsulfuration pathway activity

Duchenne muscular dystrophy (DMD) is the most frequent X chromosome-linked disease caused by mutations in the gene encoding for dystrophin, leading to progressive and unstoppable degeneration of skeletal muscle tissues. Despite recent advances in the understanding of the molecular processes involved in the pathogenesis of DMD, there is still no cure. In this study, we aim at investigating the potential involvement of the transsulfuration pathway (TSP), and its by-end product namely hydrogen sulfide (H2S), in primary human myoblasts isolated from DMD donors and skeletal muscles of dystrophic (mdx) mice. In myoblasts of DMD donors, we demonstrate that the expression of key genes regulating the H2S production and TSP activity, including cystathionine γ lyase (CSE), cystathionine beta-synthase (CBS), 3 mercaptopyruvate sulfurtransferase (3-MST), cysteine dioxygenase (CDO), cysteine sulfonic acid decarboxylase (CSAD), glutathione synthase (GS) and γ -glutamylcysteine synthetase (γ-GCS) is reduced. Starting from these findings, using Nuclear Magnetic Resonance (NMR) and quantitative Polymerase Chain Reaction (qPCR) we show that the levels of TSP-related metabolites such as methionine, glycine, glutathione, glutamate and taurine, as well as the expression levels of the aforementioned TSP related genes, are significantly reduced in skeletal muscles of mdx mice compared to healthy controls, at both an early (7 weeks) and overt (17 weeks) stage of the disease. Importantly, the treatment with sodium hydrosulfide (NaHS), a commonly used H2S donor, fully recovers the impaired locomotor activity in both 7 and 17 old mdx mice. This is an effect attributable to the reduced expression of pro-inflammatory markers and restoration of autophagy in skeletal muscle tissues. In conclusion, our study uncovers a defective TSP pathway activity in DMD and highlights the role of H2S-donors for novel and safe adjuvant therapy to treat symptoms of DMD