Transient interfacial tension and dilatational rheology of diffuse polymer-polymer interfaces

We demonstrate the influence of molecular weight and molecular weightasymmetry across an interface on the transient behavior of the interfacial tension. The interfacial tension was measured as a function of time for a range of polymer combinations with a broadrange of interfacial properties using a pendant/ sessile drop apparatus. The results show that neglecting mutual solubility, assumed to be a reasonable approximation in many cases, very often does not sustain. Instead, a diffuse interface layer develops in time with a corresponding transient interfacial tension. Depending on the specific combination of polymers, the transient interfacial tension is found to increase or decrease with time. The results are interpreted in terms of a recently proposed model\cite{Shi_etal2004}, giving relativecharacteristic diffusion time scales in terms of molecular weight, molecular weight distribution and viscosities. However, the time scales obtained from this theoretical approach do not give a conclusive trend. Using oscillatory dilatational interfacial experiments the viscoelastic behavior of these diffusive interfaces is demonstrated. The time evolution of the interfacial tension and thedilatational elasticity show the same trend aspredicted by the theory of diffuse interfaces, supporting the idea that the polymer combinations under consideration indeed form diffuse interfaces. The dilatational elasticity and the dilatationalviscosity show a frequency dependency that is described qualitatively by a simple Fickian diffusion model and quantitatively by a Maxwell model. The characteristic diffusion times provided by the lattershow that the systems with thick interfaces (tens of micrometers and more) can be considered as slowdiffusive systems while the systems with thinner interfaces (a few micrometers and less) can be considered as fast diffusive systems

TRIANGULATION OF THE INTERSTELLAR MAGNETIC FIELD

Determining the direction of the local interstellar magnetic field (LISMF) is important for understanding the heliosphere's global structure, the properties of the interstellar medium, and the propagation of cosmic rays in the local galactic medium. Measurements of interstellar neutral atoms by Ulysses for He and by SOHO/SWAN for H provided some of the first observational insights into the LISMF direction. Because secondary neutral H is partially deflected by the interstellar flow in the outer heliosheath and this deflection is influenced by the LISMF, the relative deflection of H versus He provides a plane—the so-called B–V plane in which the LISMF direction should lie. Interstellar Boundary Explorer (IBEX) subsequently discovered a ribbon, the center of which is conjectured to be the LISMF direction. The most recent He velocity measurements from IBEX and those from Ulysses yield a B–V plane with uncertainty limits that contain the centers of the IBEX ribbon at 0.7–2.7 keV. The possibility that Voyager 1 has moved into the outer heliosheath now suggests that Voyager 1's direct observations provide another independent determination of the LISMF. We show that LISMF direction measured by Voyager 1 is >40° off from the IBEX ribbon center and the B–V plane. Taking into account the temporal gradient of the field direction measured by Voyager 1, we extrapolate to a field direction that passes directly through the IBEX ribbon center (0.7–2.7 keV) and the B–V plane, allowing us to triangulate the LISMF direction and estimate the gradient scale size of the magnetic field

Scaling of the Conductivity with Temperature and Uniaxial Stress in Si:B at the Metal-Insulator Transition

Using uniaxial stress to tune Si:B through the metal-insulator transition we find the conductivity at low temperatures shows an excellent fit to scaling with temperature and stress on both sides of the transition. The scaling functions yield the conductivity in the metallic and insulating phases, and allow a reliable determination of the temperature dependence in the critical regions on both sides of the transition

Clinical significance of VEGF-A, -C and -D expression in esophageal malignancies

Vascular endothelial growth factors ( VEGF)- A, - C and - D are members of the proangiogenic VEGF family of glycoproteins. VEGF-A is known to be the most important angiogenic factor under physiological and pathological conditions, while VEGF-C and VEGF-D are implicated in the development and sprouting of lymphatic vessels, so called lymphangiogenesis. Local tumor progression, lymph node metastases and hematogenous tumor spread are important prognostic factors for esophageal carcinoma ( EC), one of the most lethal malignancies throughout the world. We found solid evidence in the literature that VEGF expression contributes to tumor angiogenesis, tumor progression and lymph node metastasis in esophageal squamous cell carcinoma ( SCC), and many authors could show a prognostic value for VEGF-assessment. In adenocarcinoma (AC) of the esophagus angiogenic properties are acquired in early stages, particularly in precancerous lesions like Barrett's dysplasia. However, VEGF expression fails to give prognostic information in AC of the esophagus. VEGF-C and VEGF-D were detected in SCC and dysplastic lesions, but not in normal mucosa of the esophagus. VEGF-C expression might be associated with lymphatic tumor invasion, lymph node metastases and advanced disease in esophageal SCC and AC. Therapeutic interference with VEGF signaling may prove to be a promising way of anti-angiogenic co-treatment in esophageal carcinoma. However, concrete clinical data are still pending

Systemic proteasome inhibition triggers neurodegeneration in a transgenic mouse model expressing human α-synuclein under oligodendrocyte promoter: implications for multiple system atrophy

Multiple system atrophy (MSA) is a progressive late onset neurodegenerative α-synucleinopathy with unclear pathogenesis. Recent genetic and pathological studies support a central role of α-synuclein (αSYN) in MSA pathogenesis. Oligodendroglial cytoplasmic inclusions of fibrillar αSYN and dysfunction of the ubiquitin–proteasome system are suggestive of proteolytic stress in this disorder. To address the possible pathogenic role of oligodendroglial αSYN accumulation and proteolytic failure in MSA we applied systemic proteasome inhibition (PSI) in transgenic mice with oligodendroglial human αSYN expression and determined the presence of MSA-like neurodegeneration in this model as compared to wild-type mice. PSI induced open field motor disability in transgenic αSYN mice but not in wild-type mice. The motor phenotype corresponded to progressive and selective neuronal loss in the striatonigral and olivopontocerebellar systems of PSI-treated transgenic αSYN mice. In contrast no neurodegeneration was detected in PSI-treated wild-type controls. PSI treatment of transgenic αSYN mice was associated with significant ultrastructural alterations including accumulation of fibrillar human αSYN in the cytoplasm of oligodendroglia, which resulted in myelin disruption and demyelination characterized by increased g-ratio. The oligodendroglial and myelin pathology was accompanied by axonal degeneration evidenced by signs of mitochondrial stress and dysfunctional axonal transport in the affected neurites. In summary, we provide new evidence supporting a primary role of proteolytic failure and suggesting a neurodegenerative pathomechanism related to disturbed oligodendroglial/myelin trophic support in the pathogenesis of MSA

Structural constraints revealed in consistent nucleosome positions in the genome of S. cerevisiae

<p>Abstract</p> <p>Background</p> <p>Recent advances in the field of high-throughput genomics have rendered possible the performance of genome-scale studies to define the nucleosomal landscapes of eukaryote genomes. Such analyses are aimed towards providing a better understanding of the process of nucleosome positioning, for which several models have been suggested. Nevertheless, questions regarding the sequence constraints of nucleosomal DNA and how they may have been shaped through evolution remain open. In this paper, we analyze in detail different experimental nucleosome datasets with the aim of providing a hypothesis for the emergence of nucleosome-forming sequences.</p> <p>Results</p> <p>We compared the complete sets of nucleosome positions for the budding yeast (<it>Saccharomyces cerevisiae</it>) as defined in the output of two independent experiments with the use of two different experimental techniques. We found that < 10% of the experimentally defined nucleosome positions were consistently positioned in both datasets. This subset of well-positioned nucleosomes, when compared with the bulk, was shown to have particular properties at both sequence and structural levels. Consistently positioned nucleosomes were also shown to occur preferentially in pairs of dinucleosomes, and to be surprisingly less conserved compared with their adjacent nucleosome-free linkers.</p> <p>Conclusion</p> <p>Our findings may be combined into a hypothesis for the emergence of a weak nucleosome-positioning code. According to this hypothesis, consistent nucleosomes may be partly guided by nearby nucleosome-free regions through statistical positioning. Once established, a set of well-positioned consistent nucleosomes may impose secondary constraints that further shape the structure of the underlying DNA. We were able to capture these constraints through the application of a recently introduced structural property that is related to the symmetry of DNA curvature. Furthermore, we found that both consistently positioned nucleosomes and their adjacent nucleosome-free regions show an increased tendency towards conservation of this structural feature.</p