Breakdown of step-flow growth in unstable homoepitaxy

Two mechanisms for the breakdown of step flow growth, in the sense of the appearance of steps of opposite sign to the original vicinality, are studied by kinetic Monte Carlo simulations and scaling arguments. The first mechanism is the nucleation of islands on the terraces, which leads to mound formation if interlayer transport is sufficiently inhibited. The second mechanism is the formation of vacancy islands due to the self-crossing of strongly meandering steps. The competing roles of the growth of the meander amplitude and the synchronization of the meander phase are emphasized. The distance between vacancy islands along the step direction appears to be proportional to the square of the meander wavelengthComment: 7 pages, 9 figure

A truncated laminin chain homologous to the B2 chain: structure, spatial expression, and chromosomal assignment

We describe the identification of a novel laminin chain. Overlapping clones were isolated from a human fibrosarcoma HT1080 cell cDNA library spanning a total of 5,200 bp. A second set of clones contained an alternative 3' end sequence giving a total of 4,316 bp. The longer sequence contained an open reading frame for a 1,193-residue-long polypeptide. The alternative sequence was shortened at the carboxyl-terminal end coding for a 1,111-residue-long polypeptide. The amino acid sequence contained 21 amino acids of a putative signal peptide and 1,172 residues or alternatively 1,090 residues of a sequence with five distinct domains homologous to domains I-V in laminin chains. Comparison of the amino acid sequences showed that the novel laminin chain is homologous to the laminin B2 chain. However, the structure of the novel laminin chain isolated here differs significantly from that of the B2 chain in that it has no domain VI and domains V, IV, and III are shorter, resulting in a truncated laminin chain. The alternative sequence had a shortened domain I/II. In accordance with the current nomenclature, the chain characterized here is termed B2t. Calculation of possible chain interactions of laminin chains with the B2t chain domain I/II indicated that the B2t chain can replace the B2 chain in some laminin molecules. The gene for the laminin B2t chain (LAMB2T) was localized to chromosome 1q25-q31 in close proximity to the laminin B2 chain gene. Northern analysis showed that the B2t chain is expressed in several human fetal tissues but differently from the laminin B1 and B2 chains. By in situ hybridization expression of the B2t chain was localized to specific epithelial cells in skin, lung, and kidney as opposed to a general epithelial and endothelial cell expression of the laminin B2 chain in the same tissues

Morphology of ledge patterns during step flow growth of metal surfaces vicinal to fcc(001)

The morphological development of step edge patterns in the presence of meandering instability during step flow growth is studied by simulations and numerical integration of a continuum model. It is demonstrated that the kink Ehrlich-Schwoebel barrier responsible for the instability leads to an invariant shape of the step profiles. The step morphologies change with increasing coverage from a somewhat triangular shape to a more flat, invariant steady state form. The average pattern shape extracted from the simulations is shown to be in good agreement with that obtained from numerical integration of the continuum theory.Comment: 4 pages, 4 figures, RevTeX 3, submitted to Phys. Rev.

Competing mechanisms for step meandering in unstable growth

The meander instability of a vicinal surface growing under step flow conditions is studied within a solid-on-solid model. In the absence of edge diffusion the selected meander wavelength agrees quantitatively with the continuum linear stability analysis of Bales and Zangwill [Phys. Rev. B {\bf 41}, 4400 (1990)]. In the presence of edge diffusion a local instability mechanism related to kink rounding barriers dominates, and the meander wavelength is set by one-dimensional nucleation. The long-time behavior of the meander amplitude differs in the two cases, and disagrees with the predictions of a nonlinear step evolution equation [O. Pierre-Louis et al., Phys. Rev. Lett. {\bf 80}, 4221 (1998)]. The variation of the meander wavelength with the deposition flux and with the activation barriers for step adatom detachment and step crossing (the Ehrlich-Schwoebel barrier) is studied in detail. The interpretation of recent experiments on surfaces vicinal to Cu(100) [T. Maroutian et al., Phys. Rev. B {\bf 64}, 165401 (2001)] in the light of our results yields an estimate for the kink barrier at the close packed steps.Comment: 8 pages, 7 .eps figures. Final version. Some errors in chapter V correcte

Asymptotic step profiles from a nonlinear growth equation for vicinal surfaces

We study a recently proposed nonlinear evolution equation describing the collective step meander on a vicinal surface subject to the Bales-Zangwill growth instability [O. Pierre-Louis et al., Phys. Rev. Lett. (80), 4221 (1998)]. A careful numerical analysis shows that the dynamically selected step profile consists of sloped segments, given by an inverse error function and steepening as sqrt(t), which are matched to pieces of a stationary (time-independent) solution describing the maxima and minima. The effect of smoothening by step edge diffusion is included heuristically, and a one-parameter family of evolution equations is introduced which contains relaxation by step edge diffusion and by attachment-detachment as special cases. The question of the persistence of an initially imposed meander wavelength is investigated in relation to recent experiments.Comment: 4 pages, 5 included figures. Typo in Eq.(5) corrected, section headlines added and Ref.[12] update

Local behavior of p-harmonic Green's functions in metric spaces

We describe the behavior of p-harmonic Green's functions near a singularity in metric measure spaces equipped with a doubling measure and supporting a Poincar\'e inequality

A mouse model of the schizophrenia-associated 1q21.1 microdeletion syndrome exhibits altered mesolimbic dopamine transmission

Abstract 1q21.1 hemizygous microdeletion is a copy number variant leading to eightfold increased risk of schizophrenia. In order to investigate biological alterations induced by this microdeletion, we generated a novel mouse model (Df(h1q21)/+) and characterized it in a broad test battery focusing on schizophrenia-related assays. Df(h1q21)/+ mice displayed increased hyperactivity in response to amphetamine challenge and increased sensitivity to the disruptive effects of amphetamine and phencyclidine hydrochloride (PCP) on prepulse inhibition. Probing of the direct dopamine (DA) pathway using the DA D1 receptor agonist SKF-81297 revealed no differences in induced locomotor activity compared to wild-type mice, but Df(h1q21)/+ mice showed increased sensitivity to the DA D2 receptor agonist quinpirole and the D1/D2 agonist apomorphine. Electrophysiological characterization of DA neuron firing in the ventral tegmental area revealed more spontaneously active DA neurons and increased firing variability in Df(h1q21)/+ mice, and decreased feedback reduction of DA neuron firing in response to amphetamine. In a range of other assays, Df(h1q21)/+ mice showed no difference from wild-type mice: gross brain morphology and basic functions such as reflexes, ASR, thermal pain sensitivity, and motor performance were unaltered. Similarly, anxiety related measures, baseline prepulse inhibition, and seizure threshold were unaltered. In addition to the central nervous system-related phenotypes, Df(h1q21)/+ mice exhibited reduced head-to tail length, which is reminiscent of the short stature reported in humans with 1q21.1 deletion. With aspects of both construct and face validity, the Df(h1q21)/+ model may be used to gain insight into schizophrenia-relevant alterations in dopaminergic transmission

A monitoring campaign (2013-2020) of ESA's Mars Express to study interplanetary plasma scintillation

The radio signal transmitted by the Mars Express (MEX) spacecraft was observed regularly between the years 2013-2020 at X-band (8.42 GHz) using the European Very Long Baseline Interferometry (EVN) network and University of Tasmania's telescopes. We present a method to describe the solar wind parameters by quantifying the effects of plasma on our radio signal. In doing so, we identify all the uncompensated effects on the radio signal and see which coronal processes drive them. From a technical standpoint, quantifying the effect of the plasma on the radio signal helps phase referencing for precision spacecraft tracking. The phase fluctuation of the signal was determined for Mars' orbit for solar elongation angles from 0 - 180 deg. The calculated phase residuals allow determination of the phase power spectrum. The total electron content (TEC) of the solar plasma along the line of sight is calculated by removing effects from mechanical and ionospheric noises. The spectral index was determined as $-2.43 \pm 0.11$ which is in agreement with Kolomogorov's turbulence. The theoretical models are consistent with observations at lower solar elongations however at higher solar elongation ($>$160 deg) we see the observed values to be higher. This can be caused when the uplink and downlink signals are positively correlated as a result of passing through identical plasma sheets.Comment: The paper has 13 figures and one table. It has been accepted for publication in PASA and the article will receive its DOI in a week's tim

Activation of c-Jun N-Terminal Kinase (JNK) during Mitosis in Retinal Progenitor Cells

Most studies of c-Jun N-terminal Kinase (JNK) activation in retinal tissue were done in the context of neurodegeneration. In this study, we investigated the behavior of JNK during mitosis of progenitor cells in the retina of newborn rats. Retinal explants from newborn rats were kept in vitro for 3 hours and under distinct treatments. Sections of retinal explants or freshly fixed retinal tissue were used to detect JNK phosphorylation by immunohistochemistry, and were examined through both fluorescence and confocal microscopy. Mitotic cells were identified by chromatin morphology, histone-H3 phosphorylation, and location in the retinal tissue. The subcellular localization of proteins was analyzed by double staining with both a DNA marker and an antibody to each protein. Phosphorylation of JNK was also examined by western blot. The results showed that in the retina of newborn rats (P1), JNK is phosphorylated during mitosis of progenitor cells, mainly during the early stages of mitosis. JNK1 and/or JNK2 were preferentially phosphorylated in mitotic cells. Inhibition of JNK induced cell cycle arrest, specifically in mitosis. Treatment with the JNK inhibitor decreased the number of cells in anaphase, but did not alter the number of cells in either prophase/prometaphase or metaphase. Moreover, cells with aberrant chromatin morphology were found after treatment with the JNK inhibitor. The data show, for the first time, that JNK is activated in mitotic progenitor cells of developing retinal tissue, suggesting a new role of JNK in the control of progenitor cell proliferation in the retina