Disproportionation Phenomena on Free and Strained Sn/Ge(111) and Sn/Si(111) Surfaces

Distortions of the $\sqrt3\times\sqrt3$ Sn/Ge(111) and Sn/Si(111) surfaces are shown to reflect a disproportionation of an integer pseudocharge, $Q$, related to the surface band occupancy. A novel understanding of the $(3\times3)$-1U (``1 up, 2 down'') and 2U (``2 up, 1 down'') distortions of Sn/Ge(111) is obtained by a theoretical study of the phase diagram under strain. Positive strain keeps the unstrained value Q=3 but removes distorsions. Negative strain attracts pseudocharge from the valence band causing first a $(3\times3)$-2U distortion (Q=4) on both Sn/Ge and Sn/Si, and eventually a $(\sqrt3\times\sqrt3)$-3U (``all up'') state with Q=6. The possibility of a fluctuating phase in unstrained Sn/Si(111) is discussed.Comment: Revtex, 5 pages, 3 figure

Regulation of Schwann cells oncotransformation by changes in Nf2/merlin expression, Hippo/YAP signaling and DNA methylation

Schwann cell (SC) express the Neurofibromin type 2 gene (Nf2), encoding the tumor suppressor protein merlin, a cytoskeleton-associated protein regulating cell proliferation and survival. Nf2/merlin inactivation causes protein loss and leads to SC transformation into a form of benign tumor called schwannoma. Moreover, Nf2/merlin is mutated in an autosomal dominant multiple syndrome, called neurofibromatosis type 2. In line with observation that physio/mechanical cues, such as environmental challenges, may be pathogenetically relevant for SC oncotransformation, we recently showed that the exposure to electromagnetic fields (EMFs) causes changes in SC Nf2/merlin expression, cell migration, chemotactic responsivity and cytoskeleton reorganization. We showed a downstream MAPK/Erk activation, involved in SC proliferation, as well as activation of Hippo/YAP signalling commonly altered during tumorigenesis. We also showed that some genes, known to be upstream or downstream mediators of Hippo (Amotl2, Dchs, Fat, Wnt1) were changed. Further studies on rat SC oncotransformation following acute EMF exposure (0.1 T, 50 Hz, 10 min) demonstrated that the number of cells in G1 phase was increased. Focus forming analysis, after repeated exposures, showed an increase in 3D SC growth. EMF affects also the SC epigenome, as total DNA methylation, de novo DNMT and HDAC were reduced. Furthermore, RT2-profile assay evidenced that genes crucial for SCs are upregulated in EMF exposed cells. Overall, we identified some mechanisms responsible of environmental-induced SC changes toward a proliferative/migrating state, which may be pathologically relevant for nerve tumor development

Optical properties of highly n-doped germanium obtained by in situ doping and laser annealing

High n-type doping in germanium is essential for many electronic and optoelectronic applications especially for high performance Ohmic contacts, lasing and mid-infrared plasmonics. We report on the combination of in situ doping and excimer laser annealing to improve the activation of phosphorous in germanium. An activated n-doping concentration of 8.8  ×  1019 cm−3 has been achieved starting from an incorporated phosphorous concentration of 1.1  ×  1020 cm−3. Infrared reflectivity data fitted with a multi-layer Drude model indicate good uniformity over a 350 nm thick layer. Photoluminescence demonstrates clear bandgap narrowing and an increased ratio of direct to indirect bandgap emission confirming the high doping densities achieved

Mid-Infrared Plasmonic Platform Based on n-Doped Ge-on-Si: Molecular Sensing with Germanium Nano-Antennas on Si

CMOS-compatible, heavily-doped semiconductor films are very promising for applications in mid-infrared plasmonic devices because the real part of their dielectric function is negative and broadly tunable in this wavelength range. In this work we investigate n-type doped germanium epilayers grown on Si substrates. We design and realize Ge nanoantennas on Si substrates demonstrating the presence of localized plasmon resonances, and exploit them for molecular sensing in the mid-infrared

Preliminary study on the cytoarchitecture of the human parabrachial/Kolliker-fuse complex, with reference to sudden infant death syndrome and sudden intrauterine unexplained death

The parabrachial/Kolliker-Fuse complex has been defined, in different animal species, to lie in the dorsolateral part of the pontine tegmentum and to be subdivided into three well-defined regions: the medial parabrachial nucleus, the lateral parabrachial nucleus, and the Kolliker-Fuse nucleus. Experimental studies have shown that the parabrachial/Kolliker-Fuse complex is involved in a variety of functional activities and above all plays an important role in respiratory modulation. In human brainstem, the cytoarchitecture and physiology of this complex have not yet been fully characterized. The aim of the present study was to examine fetal and infant human brainstems in order to define the precise morphology of the three nuclei of the parabrachial/Kolliker-Fuse complex, and to determine whether this nervous center shows morphologic alterations in sudden infant death syndrome (SIDS) and in sudden intrauterine unexplained death (SIUD). In serial sections of 31 brainstems of subjects aged from 32 gestational wk to 10 months of life, we studied, by morphologic and morphometric analyses, the cytoarchitecture and the extension of the three nuclei of the parabrachial/Kolliker-Fuse complex. All the morphometric parameters were very similar in SIUD and SIDS cases to those of the respective control group, as shown by the absence of significant statistical differences between the two fetus and infant groups. We observed that the features of both the lateral and the medial parabrachial nuclei are largely consistent with those reported in experimental studies. In contrast, the Kolliker-Fuse nucleus appears to be more developed in human beings than in other animal species, showing a greater extension and a more complex structure, as well as subdivision into two subnuclei (compactus and dissipatus)

Neuroactive steroids influence peripheral myelination: A promising opportunity for preventing or treating age-dependent dysfunctions of peripheral nerves

The process of aging deeply influences morphological and functional parameters of peripheral nerves. The observations summarized here indicate that the deterioration of myelin occurring in the peripheral nerves during aging may be explained by the fall of the levels of the major peripheral myelin proteins [e.g., glycoprotein Po (Po) and peripheral myelin protein 22 (PMP22)]. Neuroactive steroids, such as progesterone (PROG), dihydroprogesterone (5α-DH PROG), and tetrahydroprogesterone (3α,5α-TH PROG), are able to stimulate the low expression of these two myelin proteins present in the sciatic nerve of aged male rats. Since Po and PMP22 play an important physiological role in the maintenance of the multilamellar structure of PNS myelin, we have evaluated the effect of PROG and its neuroactive derivatives, 5α-DH PROG and 3α,5α-TH PROG, on the morphological alterations of myelinated fibers in the sciatic nerve of 22-24-month-old male rats. Data obtained clearly indicate that neuroactive steroids are able to reduce aging-associated morphological abnormalities of myelin and aging-associated myelin fiber loss in the sciatic nerve. © 2003 Elsevier Ltd. All rights reserved.Peer Reviewe

Multiple sulfatase deficiency with neonatal manifestation.

Multiple Sulfatase Deficiency (MSD; OMIM 272200) is a rare autosomal recessive inborn error of metabolism caused by mutations in the sulfatase modifying factor 1 gene, encoding the formylglycine-generating enzyme (FGE), and resulting in tissue accumulation of sulfatides, sulphated glycosaminoglycans, sphingolipids and steroid sulfates. Less than 50 cases have been published so far. We report a new case of MSD presenting in the newborn period with hypotonia, apnoea, cyanosis and rolling eyes, hepato-splenomegaly and deafness. This patient was compound heterozygous for two so far undescribed SUMF1 mutations (c.191C > A; p.S64X and c.818A > G; p.D273G)