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We report the first evidence of Raman scattering from surface phonons of a pristine metal surface. Our study reveals a Raman-active surface vibrational resonance on Cu(110) with a surprisingly large scattering efficiency. With the incident photon energy close to the energy of the Cu(110) surface state electronic transition, the Raman scattering from the surface optical resonance can be significantly enhanced, while any contribution from bulk phonons is absent.

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Density-functional theory is used to explore the Si(553)-Au surface dynamics. Our study (i) reveals a complex two-stage order-disorder phase transition where with rising temperature first the ×3 order along the Si step edges and, subsequently, the ×2 order of the Au chains is lost, (ii) identifies the transient modification of the electron chemical potential during soft Au chain vibrations as instrumental for disorder at the step edge, and (iii) shows that the transition leads to a self-doping of the Si dangling-bond wire at the step edge. The calculations are corroborated by Raman measurements of surface phonon modes and explain previous electron diffraction, scanning tunneling microscopy, and surface transport data.

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We propose a quantitative and reversible method for tuning the charge localization of Au-stabilized stepped Si surfaces by site-specific hydrogenation. This is demonstrated for Si(553)-Au as a model system by combining density functional theory simulations and reflectance anisotropy spectroscopy experiments. We find that controlled H passivation is a two-step process: step-edge adsorption drives excess charge into the conducting metal chain "reservoir" and renders it insulating, while surplus H recovers metallic behavior. Our approach illustrates a route towards microscopic manipulation of the local surface charge distribution and establishes a reversible switch of site-specific chemical reactivity and magnetic properties on vicinal surfaces.

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This 42-year-old male patient voluntarily discontinued treatment for lung TBC and twenty days later developed acute paraplegia. Magnetic resonance imaging (MRI) demonstrated a large intramedullary cavity extending from T2 to the conus medullaris. Having resumed anti-TBC treatment, the patient progressed favourably, despite any change in cavity size. Tuberculous meningitis may be complicated by the appearance of intramedullary cavities by two distinct mechanisms: 1) adhesive arachnoiditis at the skull base with obstruction of Luschka and Magendie foramina, followed by hydrocephalus and hydromyelia; and 2) spinal cord arachnoiditis with the development of arachnoidal and intramedullary cysts. In either case, symptoms are of late presentation. To the best of our knowledge, this is the first report in the literature of lung tuberculosis associated with syringomyelia but without basal arachnoiditis. Acute clinical presentation with paraplegia is exceptional.

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RESUMEN

This 42-year-old male patient voluntarily discontinued treatment for lung TBC and twenty days later developed acute paraplegia. Magnetic resonance imaging (MRI) demonstrated a large intramedullary cavity extending from T2 to the conus medullaris. Having resumed anti-TBC treatment, the patient progressed favourably, despite any change in cavity size. Tuberculous meningitis may be complicated by the appearance of intramedullary cavities by two distinct mechanisms: 1) adhesive arachnoiditis at the skull base with obstruction of Luschka and Magendie foramina, followed by hydrocephalus and hydromyelia; and 2) spinal cord arachnoiditis with the development of arachnoidal and intramedullary cysts. In either case, symptoms are of late presentation. To the best of our knowledge, this is the first report in the literature of lung tuberculosis associated with syringomyelia but without basal arachnoiditis. Acute clinical presentation with paraplegia is exceptional.

RESUMEN

This 42-year-old male patient voluntarily discontinued treatment for lung TBC and twenty days later developed acute paraplegia. Magnetic resonance imaging (MRI) demonstrated a large intramedullary cavity extending from T2 to the conus medullaris. Having resumed anti-TBC treatment, the patient progressed favourably, despite any change in cavity size. Tuberculous meningitis may be complicated by the appearance of intramedullary cavities by two distinct mechanisms: 1) adhesive arachnoiditis at the skull base with obstruction of Luschka and Magendie foramina, followed by hydrocephalus and hydromyelia; and 2) spinal cord arachnoiditis with the development of arachnoidal and intramedullary cysts. In either case, symptoms are of late presentation. To the best of our knowledge, this is the first report in the literature of lung tuberculosis associated with syringomyelia but without basal arachnoiditis. Acute clinical presentation with paraplegia is exceptional.