260 research outputs found
Field-induced delocalization and Zener breakdown in semiconductor superlattices
We investigate the energy spectrum and the electron dynamics of a band in a semiconductor superlattice as a function of the electric field. Linear optical spectroscopy shows that, for high fields, the well-known localization of the Bloch states is followed by a field-induced delocalization, associated with Zener breakdown. Using time-resolved measurements, we observe Bloch oscillations in a regime where they are damped by Zener breakdown
Antiferromagnetism and d-wave superconductivity in cuprates: a uster DMFT study
We present a new approach to investigate the coexistence of
antiferromagnetism and d-wave superconductivity in the two dimensional extended
Hubbard model within a numerically exact cluster dynamical mean-field
approximation. Self-consistent solutions with two non-zero order parameters
exists in the wide range of doping level and temperatures. A linearized
equation for energy spectrum near the Fermi level have been solved. The
resulting d-wave gap has the correct magnitude and k-dependence but some
distortion compare to the pure d_{x^2-y^2} superconducting order parameter due
to the presence of underlying antiferromagnetic ordering.Comment: 4 pages, 3 figure
The Electrical-Thermal Switching in Carbon Black-Polymer Composites as a Local Effect
Following the lack of microscopic information about the intriguing well-known
electrical-thermal switching mechanism in Carbon Black-Polymer composites, we
applied atomic force microscopy in order to reveal the local nature of the
process and correlated it with the characteristics of the widely used
commercial switches. We conclude that the switching events take place in
critical interparticle tunneling junctions that carry most of the current. The
macroscopic switched state is then a result of a dynamic-stationary state of
fast switching and slow reconnection of the corresponding junctions.Comment: 14 pages, 5 figures,Typographic correctio
The mechanisms by which polyamines accelerate tumor spread
Increased polyamine concentrations in the blood and urine of cancer patients reflect the enhanced levels of polyamine synthesis in cancer tissues arising from increased activity of enzymes responsible for polyamine synthesis. In addition to their de novo polyamine synthesis, cells can take up polyamines from extracellular sources, such as cancer tissues, food, and intestinal microbiota. Because polyamines are indispensable for cell growth, increased polyamine availability enhances cell growth. However, the malignant potential of cancer is determined by its capability to invade to surrounding tissues and metastasize to distant organs. The mechanisms by which increased polyamine levels enhance the malignant potential of cancer cells and decrease anti-tumor immunity are reviewed. Cancer cells with a greater capability to synthesize polyamines are associated with increased production of proteinases, such as serine proteinase, matrix metalloproteinases, cathepsins, and plasminogen activator, which can degrade surrounding tissues. Although cancer tissues produce vascular growth factors, their deregulated growth induces hypoxia, which in turn enhances polyamine uptake by cancer cells to further augment cell migration and suppress CD44 expression. Increased polyamine uptake by immune cells also results in reduced cytokine production needed for anti-tumor activities and decreases expression of adhesion molecules involved in anti-tumor immunity, such as CD11a and CD56. Immune cells in an environment with increased polyamine levels lose anti-tumor immune functions, such as lymphokine activated killer activities. Recent investigations revealed that increased polyamine availability enhances the capability of cancer cells to invade and metastasize to new tissues while diminishing immune cells' anti-tumor immune functions
Gut mucosal DAMPs in IBD: From mechanisms to therapeutic implications
Endogenous damage-associated molecular patterns (DAMPs) are released during tissue damage and have increasingly recognized roles in the etiology of many human diseases. The inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohnâs disease (CD), are immune-mediated conditions where high levels of DAMPs are observed. DAMPs such as calprotectin (S100A8/9) have an established clinical role as a biomarker in IBD. In this review, we use IBD as an archetypal common chronic inflammatory disease to focus on the conceptual and evidential importance of DAMPs in pathogenesis and why DAMPs represent an entirely new class of targets for clinical translation. </p
- âŚ