Evolution of femtosecond laser damage in a hafnia-silica multi-layer dielectric coating.

To optimize optical coating materials, designs, and technologies for high damage resistance, understanding the growth of laser damage is of paramount importance. In this Letter, we show the evolution of femtosecond laser damage in a hafnia-silica (HfO2/SiO2) multilayer dielectric mirror coating. Depending on various spatial features of damaged sites, we identified several regimes of the laser-material interaction with varying laser fluence and incident number of pulses. A change in surface roughness has been observed only for a small number of pulses, and interestingly, a threshold number of pulses is found for nanocrack formation. We report the polarization-dependent orientation of nanocracks and their growth with an increasing number of pulses. The presented results demonstrate that the laser damage originates from the nanobumps and surface roughening, which then leads to the formation of nanocracks. The presented experimental results acknowledge the existing theoretical models in bulk dielectrics to explain the formation of nanostructures by interference of the incident laser with the scattering radiation from laser-induced inhomogeneities and growth of the field enhancement due to nanoplasma.

Unique Combination of 22q11 and 14qter Microdeletion Syndromes Detected Using Oligonucleotide Array-CGH.

We report an infant with a unique combination of 22q11 deletion syndrome and 14q terminal deletion syndrome. The proband had clinical symptoms compatible with diagnosis of 22q11 deletion syndrome: microcephaly, micrognathia, high-arched palate, hypertelorism, short palpebral fissures, square nasal root, prominent tubular nose, hypoplastic nasal alae, bulbous nasal tip, dysplastic low-set ears, short philtrum, and heart defect, but no cell-mediated immunodeficiency typical for the syndrome. G-banding and fluorescence in situ hybridization analyses revealed a karyotype 45,XY,der(14)t(14;22)(q32.3;q11.2),-22.ish del(14)(q32.33)(D14S1420-),del(22)(q11.2q11.2)(N25-). Subsequent analyses disclosed a translocation between chromosomes 14 and 22 in the proband's mother with a deleted 14q telomere. Using comparative genome hybridization on oligonucleotide-based microarray (array-CGH), the deletion at 22q11.21 in the size of ∼4.25 Mb was revealed in the proband as well as the deletion of the telomeric area at 14q32.33qter (∼3.24 Mb) in the proband and his mother. However, both the proband and his mother showed mild symptoms (microcephaly, thin lips, carp-shaped mouth) typical for patients with the described terminal 14q deletion syndrome.