SELF TRAPPED HOLE IN ALKALINE-EARTH FLUORIDES .2. HOPPING MOTION

For pt. I, see ibid., vol.6, 229 (1973). The activation energies for the hopping motion of a self trapped hole (Vk centre) have been calculated for CaF2, SrF2 and BaF2. The estimates use the well known small polaron model, together with the microscopic model used successfully for the static properties in the previous paper. The results are in reasonable agreement with observation. Unfortunately, the only data available refer to temperatures so low that simple thermal activation is not expected, and the most serious approximation appears to be the relation of the calculated and observed parameters. In CaF2 90 degrees jumps are not observed, in contrast to all simple theories. Possible explanations are discussed; chemical bonding between the Vk ions and the nearest axial anions is not adequate, but a modification of the corresponding repulsive interaction has the correct properties

SELF TRAPPED HOLE IN ALKALINE-EARTH FLUORIDES .1. STATIC PROPERTIES

Optical and spin resonance properties have been calculated for the self trapped hole (Vk centre) in CaF2, SrF2 and BaF2. The electronic properties are regarded as those of an F2- molecular ion whose internuclear spacing has been changed by the crystalline environment, and evidence is given that this is a good approximation. The spacing is obtained from a detailed lattice relaxation calculation allowing motion of many neighbours to the defect. The results are not sensitive to the different interatomic potentials used. Good agreement with experiment is obtained for optical transition energies and linewidths and for spin resonance parameters

ELECTRONIC-STRUCTURE OF V- CENTER IN MGO

The authors have investigated in detail the two models of the V- centre, where a hole is trapped at a cation vacancy. These are the model of Bartram, Swenberg and Fourn (1965), where optical transitions occur within an O- ion, and the model of Schirmer, Koidl and Reik (1974), which involves a hole hopping from one oxygen ion to another. The calculations show (i) that the hole should be self-trapped on a single oxygen, as observed, (ii) that the predictions of ground-state ionization energy and of elastic and electrical dipole moments (apart from some uncertainties in local-field corrections) agree adequately with measurements, (iii) that the transitions within an O- ion appear to account for observed structure at around 1.5 eV, both in energy and oscillator strength, and (iv) that the observed 2.3 eV band corresponds to the transition suggested by Schirmer et al. Calculations are also given for some centres related to the V- centre, V0, V(Al)- and (Na)0, again predicting optical absorption in good agreement with experiment

THEORY OF DIFFUSION OF HEAVY IMPURITIES IN ALKALI-METALS

Interatomic potentials have been developed for heavy atom impurities in alkali metal hosts, and they have been used to calculate characteristic energies for the diffusion of gold in sodium and of silver in lithium. The calculations show that, whilst most impurity atoms should be present substitutionally, the diffusion is dominated by interstitial motion for both Li-Ag and Na-Au. The large difference in observed behaviour stems from the different forms of the interatomic potentials but cannot be described simply in terms of atomic radii or electronegativity arguments. The activation energies predicted are in good quantitative agreement with experiment

The hedgehog pathway and ocular developmental anomalies.

Mutations in effectors of the hedgehog signaling pathway are responsible for a wide variety of ocular developmental anomalies. These range from massive malformations of the brain and ocular primordia, not always compatible with postnatal life, to subtle but damaging functional effects on specific eye components. This review will concentrate on the effects and effectors of the major vertebrate hedgehog ligand for eye and brain formation, Sonic hedgehog (SHH), in tissues that constitute the eye directly and also in those tissues that exert indirect influence on eye formation. After a brief overview of human eye development, the many roles of the SHH signaling pathway during both early and later morphogenetic processes in the brain and then eye and periocular primordia will be evoked. Some of the unique molecular biology of this pathway in vertebrates, particularly ciliary signal transduction, will also be broached within this developmental cellular context

The desmosome and pemphigus

Desmosomes are patch-like intercellular adhering junctions (“maculae adherentes”), which, in concert with the related adherens junctions, provide the mechanical strength to intercellular adhesion. Therefore, it is not surprising that desmosomes are abundant in tissues subjected to significant mechanical stress such as stratified epithelia and myocardium. Desmosomal adhesion is based on the Ca2+-dependent, homo- and heterophilic transinteraction of cadherin-type adhesion molecules. Desmosomal cadherins are anchored to the intermediate filament cytoskeleton by adaptor proteins of the armadillo and plakin families. Desmosomes are dynamic structures subjected to regulation and are therefore targets of signalling pathways, which control their molecular composition and adhesive properties. Moreover, evidence is emerging that desmosomal components themselves take part in outside-in signalling under physiologic and pathologic conditions. Disturbed desmosomal adhesion contributes to the pathogenesis of a number of diseases such as pemphigus, which is caused by autoantibodies against desmosomal cadherins. Beside pemphigus, desmosome-associated diseases are caused by other mechanisms such as genetic defects or bacterial toxins. Because most of these diseases affect the skin, desmosomes are interesting not only for cell biologists who are inspired by their complex structure and molecular composition, but also for clinical physicians who are confronted with patients suffering from severe blistering skin diseases such as pemphigus. To develop disease-specific therapeutic approaches, more insights into the molecular composition and regulation of desmosomes are required

Spinster Homolog 2 (Spns2) Deficiency Causes Early Onset Progressive Hearing Loss

Spinster homolog 2 (Spns2) acts as a Sphingosine-1-phosphate (S1P) transporter in zebrafish and mice, regulating heart development and lymphocyte trafficking respectively. S1P is a biologically active lysophospholipid with multiple roles in signalling. The mechanism of action of Spns2 is still elusive in mammals. Here, we report that Spns2-deficient mice rapidly lost auditory sensitivity and endocochlear potential (EP) from 2 to 3 weeks old. We found progressive degeneration of sensory hair cells in the organ of Corti, but the earliest defect was a decline in the EP, suggesting that dysfunction of the lateral wall was the primary lesion. In the lateral wall of adult mutants, we observed structural changes of marginal cell boundaries and of strial capillaries, and reduced expression of several key proteins involved in the generation of the EP (Kcnj10, Kcnq1, Gjb2 and Gjb6), but these changes were likely to be secondary. Permeability of the boundaries of the stria vascularis and of the strial capillaries appeared normal. We also found focal retinal degeneration and anomalies of retinal capillaries together with anterior eye defects in Spns2 mutant mice. Targeted inactivation of Spns2 in red blood cells, platelets, or lymphatic or vascular endothelial cells did not affect hearing, but targeted ablation of Spns2 in the cochlea using a Sox10-Cre allele produced a similar auditory phenotype to the original mutation, suggesting that local Spns2 expression is critical for hearing in mammals. These findings indicate that Spns2 is required for normal maintenance of the EP and hence for normal auditory function, and support a role for S1P signalling in hearing