Hydrogenated and deuterated iron clusters: Infrared spectra and density functional calculations

Iron clusters react sequentially with hydrogen molecules to form multiply hydrogenated products. The increases in cluster ionization potential upon reaction verify that hydrogen chemisorbs dissociatively to form iron cluster–hydride complexes, FenHm. At low source temperatures, the cluster–hydride complexes take up additional hydrogen molecules which are shown to be physisorbed onto the underlying FenHm complexes to form FenHm(H2)p species. The infrared spectra of FenHm and FenDm (n = 9–20) were obtained by the photodissociation action spectroscopic method in which depletion of the FenHm(H2)p and FenDm(D2)p species was the signature of absorption. The spectra, recorded in the 885–1090 cm−1 region, consist of several overlapping bands, each approximately 20 cm−1 in width. The dissimilarity of each FenHm(H2)p spectrum with the corresponding FenDm(D2)p spectrum indicates that the carrier involves hydrogen and is not merely due to absorption by the underlying iron cluster. Density functional calculations were performed on model complexes, Fe13H14 and Fe13D14, the iron portion of which was assumed to have Th symmetry. The infrared-active vibrational frequencies involving hydrogen bending and deuterium stretching are predicted to lie within the experimental frequency range of the experiment, well removed from the skeletal modes of the underlying iron cluster. The complexity of the observed spectra as compared to simulations based on the assumed (high-symmetry) model imply that the experimentally produced complexes possess low symmetry

Work functions, ionization potentials, and in-between: Scaling relations based on the image charge model

We revisit a model in which the ionization energy of a metal particle is associated with the work done by the image charge force in moving the electron from infinity to a small cut-off distance just outside the surface. We show that this model can be compactly, and productively, employed to study the size dependence of electron removal energies over the range encompassing bulk surfaces, finite clusters, and individual atoms. It accounts in a straightforward manner for the empirically known correlation between the atomic ionization potential (IP) and the metal work function (WF), IP/WF$\sim$2. We formulate simple expressions for the model parameters, requiring only a single property (the atomic polarizability or the nearest neighbor distance) as input. Without any additional adjustable parameters, the model yields both the IP and the WF within $\sim$10% for all metallic elements, as well as matches the size evolution of the ionization potentials of finite metal clusters for a large fraction of the experimental data. The parametrization takes advantage of a remarkably constant numerical correlation between the nearest-neighbor distance in a crystal, the cube root of the atomic polarizability, and the image force cutoff length. The paper also includes an analytical derivation of the relation of the outer radius of a cluster of close-packed spheres to its geometric structure.Comment: Original submission: 8 pages with 7 figures incorporated in the text. Revised submission (added one more paragraph about alloy work functions): 18 double spaced pages + 8 separate figures. Accepted for publication in PR

Ferromagnetic behavior of ultrathin manganese nanosheets

Ferromagnetic behaviour has been observed experimentally for the first time in nanostructured Manganese. Ultrathin ($\sim$ 0.6 nm) Manganese nanosheets have been synthesized inside the two dimensional channels of sol-gel derived Na-4 mica. The magnetic properties of the confined system are measured within 2K-300K temperature range. The confined structure is found to show a ferromagnetic behaviour with a nonzero coercivity value. The coercivity value remains positive throughout the entire temperature range of measurement. The experimental variation of susceptibility as a function of temperature has been satisfactorily explained on the basis of a two dimensional system with a Heisenberg Hamiltonian involving direct exchange interaction.Comment: 13 pages, 9 figure

CO adsorption on neutral iridium clusters

The adsorption of carbon monoxide on neutral iridium clusters in the size range of n = 3 to 21 atoms is investigated with infrared multiple photon dissociation spectroscopy. For each cluster size only a single v(CO) band is present with frequencies in the range between 1962 cm-1 (n = 8) and 1985 cm-1 (n = 18) which can be attributed to an atop binding geometry. This behaviour is compared to the CO binding geometries on clusters of other group 9 and 10 transition metals as well as to that on extended surfaces. The preference of Ir for atop binding is rationalized by relativistic effects on the electronic structure of the later 5d metals

Whole Genome Sequencing Identified a 16 Kilobase Deletion on ECA13 Associated with Distichiasis in Friesian Horses

BACKGROUND: Distichiasis, an ocular disorder in which aberrant cilia (eyelashes) grow from the opening of the Meibomian glands of the eyelid, has been reported in Friesian horses. These misplaced cilia can cause discomfort, chronic keratitis, and corneal ulceration, potentially impacting vision due to corneal fibrosis, or, if secondary infection occurs, may lead to loss of the eye. Friesian horses represent the vast majority of reported cases of equine distichiasis, and as the breed is known to be affected with inherited monogenic disorders, this condition was hypothesized to be a simply inherited Mendelian trait. RESULTS: A genome wide association study (GWAS) was performed using the Axiom 670 k Equine Genotyping array (MNEc670k) utilizing 14 cases and 38 controls phenotyped for distichiasis. An additive single locus mixed linear model (EMMAX) approach identified a 1.83 Mb locus on ECA5 and a 1.34 Mb locus on ECA13 that reached genome-wide significance (pcorrected = 0.016 and 0.032, respectively). Only the locus on ECA13 withstood replication testing (p = 1.6 × 10− 5, cases: n = 5 and controls: n = 37). A 371 kb run of homozygosity (ROH) on ECA13 was found in 13 of the 14 cases, providing evidence for a recessive mode of inheritance. Haplotype analysis (hapQTL) narrowed the region of association on ECA13 to 163 kb. Whole-genome sequencing data from 3 cases and 2 controls identified a 16 kb deletion within the ECA13 associated haplotype (ECA13:g.178714_195130del). Functional annotation data supports a tissue-specific regulatory role of this locus. This deletion was associated with distichiasis, as 18 of the 19 cases were homozygous (p = 4.8 × 10− 13). Genotyping the deletion in 955 horses from 54 different breeds identified the deletion in only 11 non-Friesians, all of which were carriers, suggesting that this could be causal for this Friesian disorder. CONCLUSIONS: This study identified a 16 kb deletion on ECA13 in an intergenic region that was associated with distichiasis in Friesian horses. Further functional analysis in relevant tissues from cases and controls will help to clarify the precise role of this deletion in normal and abnormal eyelash development and investigate the hypothesis of incomplete penetrance

Unified description of magic numbers of metal clusters in terms of the 3-dimensional q-deformed harmonic oscillator

Magic numbers predicted by a 3-dimensional q-deformed harmonic oscillator with Uq(3)>SOq(3) symmetry are compared to experimental data for atomic clusters of alkali metals (Li, Na, K, Rb, Cs), noble metals (Cu, Ag, Au), divalent metals (Zn, Cd), and trivalent metals (Al, In), as well as to theoretical predictions of jellium models, Woods-Saxon and wine bottle potentials, and to the classification scheme using the 3n+l pseudo quantum number. In alkali metal clusters and noble metal clusters the 3-dimensional q-deformed harmonic oscillator correctly predicts all experimentally observed magic numbers up to 1500 (which is the expected limit of validity for theories based on the filling of electronic shells), while in addition it gives satisfactory results for the magic numbers of clusters of divalent metals and trivalent metals, thus indicating that Uq(3), which is a nonlinear extension of the U(3) symmetry of the spherical (3-dimensional isotropic) harmonic oscillator, is a good candidate for being the symmetry of systems of several metal clusters. The Taylor expansions of angular momentum dependent potentials approximately producing the same spectrum as the 3-dimensional q-deformed harmonic oscillator are found to be similar to the Taylor expansions of the symmetrized Woods-Saxon and wine-bottle symmetrized Woods-Saxon potentials, which are known to provide successful fits of the Ekardt potentials.Comment: 23 pages including 7 table

A hematopoietic contribution to microhemorrhage formation during antiviral CD8 T cell-initiated blood-brain barrier disruption

<p>Abstract</p> <p>Background</p> <p>The extent to which susceptibility to brain hemorrhage is derived from blood-derived factors or stromal tissue remains largely unknown. We have developed an inducible model of CD8 T cell-initiated blood-brain barrier (BBB) disruption using a variation of the Theiler's murine encephalomyelitis virus (TMEV) model of multiple sclerosis. This peptide-induced fatal syndrome (PIFS) model results in severe central nervous system (CNS) vascular permeability and death in the C57BL/6 mouse strain, but not in the 129 SvIm mouse strain, despite the two strains' having indistinguishable CD8 T-cell responses. Therefore, we hypothesize that hematopoietic factors contribute to susceptibility to brain hemorrhage, CNS vascular permeability and death following induction of PIFS.</p> <p>Methods</p> <p>PIFS was induced by intravenous injection of VP2_121-130peptide at 7 days post-TMEV infection. We then investigated brain inflammation, astrocyte activation, vascular permeability, functional deficit and microhemorrhage formation using T2*-weighted magnetic resonance imaging (MRI) in C57BL/6 and 129 SvIm mice. To investigate the contribution of hematopoietic cells in this model, hemorrhage-resistant 129 SvIm mice were reconstituted with C57BL/6 or autologous 129 SvIm bone marrow. Gadolinium-enhanced, T1-weighted MRI was used to visualize the extent of CNS vascular permeability after bone marrow transfer.</p> <p>Results</p> <p>C57BL/6 and 129 SvIm mice had similar inflammation in the CNS during acute infection. After administration of VP2_121-130peptide, however, C57BL/6 mice had increased astrocyte activation, CNS vascular permeability, microhemorrhage formation and functional deficits compared to 129 SvIm mice. The 129 SvIm mice reconstituted with C57BL/6 but not autologous bone marrow had increased microhemorrhage formation as measured by T2*-weighted MRI, exhibited a profound increase in CNS vascular permeability as measured by three-dimensional volumetric analysis of gadolinium-enhanced, T1-weighted MRI, and became moribund in this model system.</p> <p>Conclusion</p> <p>C57BL/6 mice are highly susceptible to microhemorrhage formation, severe CNS vascular permeability and morbidity compared to the 129 SvIm mouse. This susceptibility is transferable with the bone marrow compartment, demonstrating that hematopoietic factors are responsible for the onset of brain microhemorrhage and vascular permeability in immune-mediated fatal BBB disruption.</p

Local CD4 and CD8 T-Cell Reactivity to HSV-1 Antigens Documents Broad Viral Protein Expression and Immune Competence in Latently Infected Human Trigeminal Ganglia

Herpes simplex virus type 1 (HSV-1) infection results in lifelong chronic infection of trigeminal ganglion (TG) neurons, also referred to as neuronal HSV-1 latency, with periodic reactivation leading to recrudescent herpetic disease in some persons. HSV-1 proteins are expressed in a temporally coordinated fashion during lytic infection, but their expression pattern during latent infection is largely unknown. Selective retention of HSV-1 reactive T-cells in human TG suggests their role in controlling reactivation by recognizing locally expressed HSV-1 proteins. We characterized the HSV-1 proteins recognized by virus-specific CD4 and CD8 T-cells recovered from human HSV-1-infected TG. T-cell clusters, consisting of both CD4 and CD8 T-cells, surrounded neurons and expressed mRNAs and proteins consistent with in situ antigen recognition and antiviral function. HSV-1 proteome-wide scans revealed that intra-TG T-cell responses included both CD4 and CD8 T-cells directed to one to three HSV-1 proteins per person. HSV-1 protein ICP6 was targeted by CD8 T-cells in 4 of 8 HLA-discordant donors. In situ tetramer staining demonstrated HSV-1-specific CD8 T-cells juxtaposed to TG neurons. Intra-TG retention of virus-specific CD4 T-cells, validated to the HSV-1 peptide level, implies trafficking of viral proteins from neurons to HLA class II-expressing non-neuronal cells for antigen presentation. The diversity of viral proteins targeted by TG T-cells across all kinetic and functional classes of viral proteins suggests broad HSV-1 protein expression, and viral antigen processing and presentation, in latently infected human TG. Collectively, the human TG represents an immunocompetent environment for both CD4 and CD8 T-cell recognition of HSV-1 proteins expressed during latent infection. HSV-1 proteins recognized by TG-resident T-cells, particularly ICP6 and VP16, are potential HSV-1 vaccine candidates

Neurons are MHC Class I-Dependent Targets for CD8 T Cells upon Neurotropic Viral Infection

Following infection of the central nervous system (CNS), the immune system is faced with the challenge of eliminating the pathogen without causing significant damage to neurons, which have limited capacities of renewal. In particular, it was thought that neurons were protected from direct attack by cytotoxic T lymphocytes (CTL) because they do not express major histocompatibility class I (MHC I) molecules, at least at steady state. To date, most of our current knowledge on the specifics of neuron-CTL interaction is based on studies artificially inducing MHC I expression on neurons, loading them with exogenous peptide and applying CTL clones or lines often differentiated in culture. Thus, much remains to be uncovered regarding the modalities of the interaction between infected neurons and antiviral CD8 T cells in the course of a natural disease. Here, we used the model of neuroinflammation caused by neurotropic Borna disease virus (BDV), in which virus-specific CTL have been demonstrated as the main immune effectors triggering disease. We tested the pathogenic properties of brain-isolated CD8 T cells against pure neuronal cultures infected with BDV. We observed that BDV infection of cortical neurons triggered a significant up regulation of MHC I molecules, rendering them susceptible to recognition by antiviral CTL, freshly isolated from the brains of acutely infected rats. Using real-time imaging, we analyzed the spatio-temporal relationships between neurons and CTL. Brain-isolated CTL exhibited a reduced mobility and established stable contacts with BDV-infected neurons, in an antigen- and MHC-dependent manner. This interaction induced rapid morphological changes of the neurons, without immediate killing or impairment of electrical activity. Early signs of neuronal apoptosis were detected only hours after this initial contact. Thus, our results show that infected neurons can be recognized efficiently by brain-isolated antiviral CD8 T cells and uncover the unusual modalities of CTL-induced neuronal damage