Laser anneal of oxycarbosilane low-k film

Submilisecond laser anneal has been experimentally investigated for porogen removal and its ability to improve the mechanical strength in oxycarbosilane ultra low-k films compromised due to the introduction of porosity. We report the occurrence of extensive bond rearrangements inferred from Fourier-transform infra-red (FTIR) spectroscopy, elastic recoil detection (ERD) and spectroscopic ellipsometry (SE) in the energy range of 1.4-8 eV. The laser anneal affects most notably the organic content of the organosilicate matrix leading to depletion and reorganization. Nevertheless, the tested conditions reveal a processing window which allows for 13% improvement of Young’s modulus as compared to the reference film, annealed in a conventional furnace at 400°C for 2 h, while not impacting the relative dielectric constant of 2.25

Reorientation of Spin Density Waves in Cr(001) Films induced by Fe(001) Cap Layers

Proximity effects of 20 \AA thin Fe layers on the spin density waves (SDWs) in epitaxial Cr(001) films are revealed by neutron scattering. Unlike in bulk Cr we observe a SDW with its wave vector Q pointing along only one {100} direction which depends dramatically on the film thickness t_{Cr}. For t_{Cr} < 250 \AA the SDW propagates out-of-plane with the spins in the film plane. For t_{Cr} > 1000 \AA the SDW propagates in the film plane with the spins out-of-plane perpendicular to the in-plane Fe moments. This reorientation transition is explained by frustration effects in the antiferromagnetic interaction between Fe and Cr across the Fe/Cr interface due to steps at the interface.Comment: 4 pages (RevTeX), 3 figures (EPS

Morphological changes in the Scheldt estuary and its consequences on hydrodynamics

This paper starts with a brief physical description of the estuary and a summary of its historical developments, with emphasis on human interference, such as the loss of storage area in the basin, sediment circulation by dredging and dumping, etc. Next, the various relevant hydrodynamic processes are described, responsible for the morphodynamic development of the estuary: -tidal asymmetry, length of ebb and flood period, length of HWS and LWS-period, and -effect of the hypsometry (cross sectional shape of the estuary) on the tidal propagation. The impact of morphological changes on the overall tidal movement and on the overtides is treated in the last two sections of the paper. Where possible, the interaction between morphological changes and water movement is discussed

Mitochondrial mosaics in the liver of 3 infants with mtDNA defects

<p>Abstract</p> <p>Background</p> <p>In muscle cytochrome oxidase (COX) negative fibers (mitochondrial mosaics) have often been visualized.</p> <p>Methods</p> <p>COX activity staining of liver for light and electron microscopy, muscle stains, blue native gel electrophoresis and activity assays of respiratory chain proteins, their immunolocalisation, mitochondrial and nuclear DNA analysis.</p> <p>Results</p> <p>Three unrelated infants showed a mitochondrial mosaic in the liver after staining for COX activity, i.e. hepatocytes with strongly reactive mitochondria were found adjacent to cells with many negative, or barely reactive, mitochondria. Deficiency was most severe in the patient diagnosed with Pearson syndrome. Ragged-red fibers were absent in muscle biopsies of all patients. Enzyme biochemistry was not diagnostic in muscle, fibroblasts and lymphocytes. Blue native gel electrophoresis of liver tissue, but not of muscle, demonstrated a decreased activity of complex IV; in both muscle and liver subcomplexes of complex V were seen. Immunocytochemistry of complex IV confirmed the mosaic pattern in two livers, but not in fibroblasts. MRI of the brain revealed severe white matter cavitation in the Pearson case, but only slight cortical atrophy in the Alpers-Huttenlocher patient, and a normal image in the 3rd. MtDNA in leucocytes showed a common deletion in 50% of the mtDNA molecules of the Pearson patient. In the patient diagnosed with Alpers-Huttenlocher syndrome, mtDNA was depleted for 60% in muscle. In the 3rd patient muscular and hepatic mtDNA was depleted for more than 70%. Mutations in the nuclear encoded gene of <it>POLG </it>were subsequently found in both the 2nd and 3rd patients.</p> <p>Conclusion</p> <p>Histoenzymatic COX staining of a liver biopsy is fast and yields crucial data about the pathogenesis; it indicates whether mtDNA should be assayed. Each time a mitochondrial disorder is suspected and muscle data are non-diagnostic, a liver biopsy should be recommended. Mosaics are probably more frequent than observed until now. A novel pathogenic mutation in <it>POLG </it>is reported.</p> <p>Tentative explanations for the mitochondrial mosaics are, in one patient, unequal partition of mutated mitochondria during mitoses, and in two others, an interaction between products of several genes required for mtDNA maintenance.</p