Spatio-temporal distribution of nucleation events during crystal growth

We consider irreversible second-layer nucleation that occurs when two adatoms on a terrace meet. We solve the problem analytically in one dimension for zero and infinite step-edge barriers, and numerically for any value of the barriers in one and two dimensions. For large barriers, the spatial distribution of nucleation events strongly differs from $\rho^2$, where $\rho$ is the stationary adatom density in the presence of a constant flux. The probability $Q(t)$ that nucleation occurs at time $t$ after the deposition of the second adatom, decays for short time as a power law [$Q(t)\sim t^{-1/2}$] in $d=1$ and logarithmically [$Q(t)\sim 1/\ln(t/t_0)$] in $d=2$; for long time it decays exponentially. Theories of the nucleation rate $\omega$ based on the assumption that it is proportional to $\rho^2$ are shown to overestimate $\omega$ by a factor proportional to the number of times an adatom diffusing on the terrace visits an already visited lattice site.Comment: 4 pages, 3 figures; accepted for publication on PR

Crater formation by fast ions: comparison of experiment with Molecular Dynamics simulations

An incident fast ion in the electronic stopping regime produces a track of excitations which can lead to particle ejection and cratering. Molecular Dynamics simulations of the evolution of the deposited energy were used to study the resulting crater morphology as a function of the excitation density in a cylindrical track for large angle of incidence with respect to the surface normal. Surprisingly, the overall behavior is shown to be similar to that seen in the experimental data for crater formation in polymers. However, the simulations give greater insight into the cratering process. The threshold for crater formation occurs when the excitation density approaches the cohesive energy density, and a crater rim is formed at about six times that energy density. The crater length scales roughly as the square root of the electronic stopping power, and the crater width and depth seem to saturate for the largest energy densities considered here. The number of ejected particles, the sputtering yield, is shown to be much smaller than simple estimates based on crater size unless the full crater morphology is considered. Therefore, crater size can not easily be used to estimate the sputtering yield.Comment: LaTeX, 7 pages, 5 EPS figures. For related figures/movies, see: http://dirac.ms.virginia.edu/~emb3t/craters/craters.html New version uploaded 5/16/01, with minor text changes + new figure

Self-diffusion along step bottoms on Pt(111)

First-principles total energies of periodic vicinals are used to estimate barriers for Pt-adatom diffusion along straight and kinked steps on Pt(111), and around a corner where straight steps intersect. In all cases studied, hopping diffusion has a lower barrier than concerted substitution. In conflict with simulations of dendritic Pt island formation on Pt(111), hopping from a corner site to a step whose riser is a (111)-micro facet is predicted to be more facile than to one whose riser is a (100)

The N-Myc Down Regulated Gene1 (NDRG1) Is a Rab4a Effector Involved in Vesicular Recycling of E-Cadherin

Cell to cell adhesion is mediated by adhesion molecules present on the cell surface. Downregulation of molecules that form the adhesion complex is a characteristic of metastatic cancer cells. Downregulation of the N-myc down regulated gene1 (NDRG1) increases prostate and breast metastasis. The exact function of NDRG1 is not known. Here by using live cell confocal microscopy and in vitro reconstitution, we report that NDRG1 is involved in recycling the adhesion molecule E-cadherin thereby stabilizing it. Evidence is provided that NDRG1 recruits on recycling endosomes in the Trans Golgi network by binding to phosphotidylinositol 4-phosphate and interacts with membrane bound Rab4aGTPase. NDRG1 specifically interacts with constitutively active Rab4aQ67L mutant protein and not with GDP-bound Rab4aS22N mutant proving NDRG1 as a novel Rab4a effector. Transferrin recycling experiments reveals NDRG1 colocalizes with transferrin during the recycling phase. NDRG1 alters the kinetics of transferrin recycling in cells. NDRG1 knockdown cells show a delay in recycling transferrin, conversely NDRG1 overexpressing cells reveal an increase in rate of transferrin recycling. This novel finding of NDRG1 as a recycling protein involved with recycling of E-cadherin will aid in understanding NDRG1 role as a metastasis suppressor protein

Genetic diversity and demographic instability in Riftia pachyptila tubeworms from eastern Pacific hydrothermal vents

<p>Abstract</p> <p>Background</p> <p>Deep-sea hydrothermal vent animals occupy patchy and ephemeral habitats supported by chemosynthetic primary production. Volcanic and tectonic activities controlling the turnover of these habitats contribute to demographic instability that erodes genetic variation within and among colonies of these animals. We examined DNA sequences from one mitochondrial and three nuclear gene loci to assess genetic diversity in the siboglinid tubeworm, <it>Riftia pachyptila</it>, a widely distributed constituent of vents along the East Pacific Rise and Galápagos Rift.</p> <p>Results</p> <p>Genetic differentiation (<it>F</it>_<it>ST</it>) among populations increased with geographical distances, as expected under a linear stepping-stone model of dispersal. Low levels of DNA sequence diversity occurred at all four loci, allowing us to exclude the hypothesis that an idiosyncratic selective sweep eliminated mitochondrial diversity alone. Total gene diversity declined with tectonic spreading rates. The southernmost populations, which are subjected to superfast spreading rates and high probabilities of extinction, are relatively homogenous genetically.</p> <p>Conclusions</p> <p>Compared to other vent species, DNA sequence diversity is extremely low in <it>R. pachyptila</it>. Though its dispersal abilities appear to be effective, the low diversity, particularly in southern hemisphere populations, is consistent with frequent local extinction and (re)colonization events.</p

Copy Number Variation in Patients with Disorders of Sex Development Due to 46,XY Gonadal Dysgenesis

Disorders of sex development (DSD), ranging in severity from mild genital abnormalities to complete sex reversal, represent a major concern for patients and their families. DSD are often due to disruption of the genetic programs that regulate gonad development. Although some genes have been identified in these developmental pathways, the causative mutations have not been identified in more than 50% 46,XY DSD cases. We used the Affymetrix Genome-Wide Human SNP Array 6.0 to analyse copy number variation in 23 individuals with unexplained 46,XY DSD due to gonadal dysgenesis (GD). Here we describe three discrete changes in copy number that are the likely cause of the GD. Firstly, we identified a large duplication on the X chromosome that included DAX1 (NR0B1). Secondly, we identified a rearrangement that appears to affect a novel gonad-specific regulatory region in a known testis gene, SOX9. Surprisingly this patient lacked any signs of campomelic dysplasia, suggesting that the deletion affected expression of SOX9 only in the gonad. Functional analysis of potential SRY binding sites within this deleted region identified five putative enhancers, suggesting that sequences additional to the known SRY-binding TES enhancer influence human testis-specific SOX9 expression. Thirdly, we identified a small deletion immediately downstream of GATA4, supporting a role for GATA4 in gonad development in humans. These CNV analyses give new insights into the pathways involved in human gonad development and dysfunction, and suggest that rearrangements of non-coding sequences disturbing gene regulation may account for significant proportion of DSD cases