Growth Mechanism of Self-Catalyzed Group III−V Nanowires

Group III-V nanowires offer the exciting possibility of epitaxial growth on a wide variety of substrates, most importantly silicon. To ensure compatibility with Si technology, catalyst-free growth schemes are of particular relevance, to avoid impurities from the catalysts. While this type of growth is well-documented and some aspects are described, no detailed understanding of the nucleation and the growth mechanism has been developed. By combining a series of growth experiments using metal-organic vapor phase epitaxy, as well as detailed in situ surface imaging and spectroscopy, we gain deeper insight into nucleation and growth of self-seeded III-V nanowires. By this mechanism most work available in literature concerning this field can be described

Seeing as sensing : the structuring of bodily experience in modern pictorial art

Two main arguments are developed in this thesis: first is the claim that our ability to make and understand representational pictures has a natural basis in our capacity to see. In this respect, I have drawn on the ideas of the visual scientist, David Marr and on the theory of representation expounded by John Willats. Second, I argue that the view articulated by these theorists forms a theoretical backdrop for, but does not satisfactorily explain, how pictures may heighten our sense of bodily presence. A central aim of this thesis is therefore to show how this mode of expression is also non-arbitrarily linked to the process of seeing by virtue of its relationship with our visuomotor capacities. In order to give substance to these ideas, I have attempted to weave together knowledge of art history with neuropsychological evidence and phenomenological philosophy. In applying this view to the work of particular artists, I have largely focussed on the oeuvre of Cézanne and the Cubists. However, the general form of this argument is intended to have wider implications, indicating the development of a stylistic tendency in modern art and showing how it differs from that of the Renaissance tradition. In conclusion, my thesis expresses the view that vision – and hence representation – can be divided along two separate lines: one related to a conceptual form of seeing and the other related to a bodily form of perception. The "crisis of representation" in the late nineteenth century is therefore considered indicative of a rejection of the former mode of visuality. Instead, modern artists are said to re-structure the viewing experience so that it shows the reliance of sight on the body, thus permitting the beholder a more active and constitutive role in the perception of art.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Boson Stars: Alternatives to primordial black holes?

The present surge for the astrophysical relevance of boson stars stems from the speculative possibility that these compact objects could provide a considerable fraction of the non-baryonic part of dark matter within the halo of galaxies. For a very light `universal' axion of effective string models, their total gravitational mass will be in the most likely range of \sim 0.5 M_\odot of MACHOs. According to this framework, gravitational microlensing is indirectly ``weighing" the axion mass, resulting in \sim 10^{-10} eV/c^2. This conclusion is not changing much, if we use a dilaton type self-interaction for the bosons. Moreover, we review their formation, rotation and stability as likely candidates of astrophysical importance.Comment: 14 pages, uses REVTeX, 1 postscript figur

Experimental discrimination of ion stopping models near the Bragg peak in highly ionized matter

The energy deposition of ions in dense plasmas is a key process in inertial confinement fusion that determines the α-particle heating expected to trigger a burn wave in the hydrogen pellet and resulting in high thermonuclear gain. However, measurements of ion stopping in plasmas are scarce and mostly restricted to high ion velocities where theory agrees with the data. Here, we report experimental data at low projectile velocities near the Bragg peak, where the stopping force reaches its maximum. This parameter range features the largest theoretical uncertainties and conclusive data are missing until today. The precision of our measurements, combined with a reliable knowledge of the plasma parameters, allows to disprove several standard models for the stopping power for beam velocities typically encountered in inertial fusion. On the other hand, our data support theories that include a detailed treatment of strong ion-electron collisions

Impaired CK1 Delta Activity Attenuates SV40-Induced Cellular Transformation In Vitro and Mouse Mammary Carcinogenesis In Vivo

Simian virus 40 (SV40) is a powerful tool to study cellular transformation in vitro, as well as tumor development and progression in vivo. Various cellular kinases, among them members of the CK1 family, play an important role in modulating the transforming activity of SV40, including the transforming activity of T-Ag, the major transforming protein of SV40, itself. Here we characterized the effects of mutant CK1δ variants with impaired kinase activity on SV40-induced cell transformation in vitro, and on SV40-induced mammary carcinogenesis in vivo in a transgenic/bi-transgenic mouse model. CK1δ mutants exhibited a reduced kinase activity compared to wtCK1δ in in vitro kinase assays. Molecular modeling studies suggested that mutation N172D, located within the substrate binding region, is mainly responsible for impaired mutCK1δ activity. When stably over-expressed in maximal transformed SV-52 cells, CK1δ mutants induced reversion to a minimal transformed phenotype by dominant-negative interference with endogenous wtCK1δ. To characterize the effects of CK1δ on SV40-induced mammary carcinogenesis, we generated transgenic mice expressing mutant CK1δ under the control of the whey acidic protein (WAP) gene promoter, and crossed them with SV40 transgenic WAP-T-antigen (WAP-T) mice. Both WAP-T mice as well as WAP-mutCK1δ/WAP-T bi-transgenic mice developed breast cancer. However, tumor incidence was lower and life span was significantly longer in WAP-mutCK1δ/WAP-T bi-transgenic animals. The reduced CK1δ activity did not affect early lesion formation during tumorigenesis, suggesting that impaired CK1δ activity reduces the probability for outgrowth of in situ carcinomas to invasive carcinomas. The different tumorigenic potential of SV40 in WAP-T and WAP-mutCK1δ/WAP-T tumors was also reflected by a significantly different expression of various genes known to be involved in tumor progression, specifically of those involved in wnt-signaling and DNA repair. Our data show that inactivating mutations in CK1δ impair SV40-induced cellular transformation in vitro and mouse mammary carcinogenesis in vivo

Chloroquine activates the p53 pathway and induces apoptosis in human glioma cells

Glioblastoma is the most common malignant brain tumor in adults. The currently available treatments offer only a palliative survival advantage and the need for effective treatments remains an urgent priority. Activation of the p53 growth suppression/apoptotic pathway is one of the promising strategies in targeting glioma cells. We show that the quinoline derivative chloroquine activates the p53 pathway and suppresses growth of glioma cells in vitro and in vivo in an orthotopic (U87MG) human glioblastoma mouse model. Induction of apoptosis is one of the mechanisms underlying the effects of chloroquine on suppressing glioma cell growth and viability. siRNA-mediated downregulation of p53 in wild-type but not mutant p53 glioblastoma cells substantially impaired chloroquine-induced apoptosis. In addition to its p53-activating effects, chloroquine may also inhibit glioma cell growth via p53-independent mechanisms. Our results clarify the mechanistic basis underlying the antineoplastic effect of chloroquine and reveal its therapeutic potential as an adjunct to glioma chemotherapy

Neuraminidase-deficient Sendai virus HN mutants provide protection from homologous superinfection

Binding of hemagglutinin-neuraminidase proteins (HN) to sialylated receptors initiates the infection process of several paramyxoviruses, whereas later in the viral life cycle, the neuramindase (NA) activity of newly synthesized HN destroys all receptors. Prior to NA action, expressed HN has to bind the receptor. To evaluate this HN–receptor complex with respect to receptor inactivation, three temperature-sensitive Sendai virus HN mutants carrying amino acid exchanges at positions 262, 264 and/or 461 were created that uncoupled NA activity from receptor binding at 39°C. Interestingly, at elevated temperature, when there is no detectable neuramindase activity, all infected cells are protected against homologous superinfection. Mutated HN protein on the cell surface is mainly bound to sialylated cell-surface components but can be released by treatment with NA. Thus, continuous binding to HN already inactivates the receptors quantitatively. Furthermore, mutant HN bound to receptors is prevented from being incorporated into virus particles in the absence of NA. It is shown here for the first time that during paramyxoviral infection, quantitative receptor inactivation already occurs due to binding of receptors to expressed HN protein without involvement of NA and is independent of NA activity of viral progeny. NA subsequently functions in the release of HN from the complex, coupled with desialysation of receptors. These findings could have implications for further antiviral drug development