Long-time self-similar asymptotic of the macroscopic quantum models

The unipolar and bipolar macroscopic quantum models derived recently for instance in the area of charge transport are considered in spatial one-dimensional whole space in the present paper. These models consist of nonlinear fourth-order parabolic equation for unipolar case or coupled nonlinear fourth-order parabolic system for bipolar case. We show for the first time the self-similarity property of the macroscopic quantum models in large time. Namely, we show that there exists a unique global strong solution with strictly positive density to the initial value problem of the macroscopic quantum models which tends to a self-similar wave (which is not the exact solution of the models) in large time at an algebraic time-decay rate.Comment: 18 page

A note on current-voltage characteristics from the quantum hydrodynamic equations for semiconductors

AbstractThe quantum hydrodynamic model is primary used for the simulation of resonant tunneling diodes. The current-voltage characteristics of these diodes show negative differential resistance (NDR) effects. For two simplified one-dimensional quantum models derived by means of asymptotic analysis, explicit formulas of the current-voltage characteristics are given. It turns out that not only the quantum correction term but also the convection term are mathematically responsible for the NDR effects. This observation is confirmed by numerical simulations of the full isothermal quantum hydrodynamic model

Algebraic time-decay for the bipolar quantum hydrodynamic model

The initial value problem is considered in the present paper for bipolar quantum hydrodynamic model for semiconductors (QHD) in $\mathbb{R}^3$. We prove that the unique strong solution exists globally in time and tends to the asymptotical state with an algebraic rate as $t\to+\infty$. And, we show that the global solution of linearized bipolar QHD system decays in time at an algebraic decay rate from both above and below. This means in general, we can not get exponential time-decay rate for bipolar QHD system, which is different from the case of unipolar QHD model (where global solutions tend to the equilibrium state at an exponential time-decay rate) and is mainly caused by the nonlinear coupling and cancelation between two carriers. Moreover, it is also shown that the nonlinear dispersion does not affect the long time asymptotic behavior, which by product gives rise to the algebraic time-decay rate of the solution of the bipolar hydrodynamical model in the semiclassical limit.Comment: 23 page

Epigentics in rheumatic diseases

The human genome comprises approximately 30000 genes needed for the formation and function of approximately 1 Million proteins in the human body. Differentiation leads to the deactivation of genes that are not needed in the specific tissues or cells. To regulate the cell specific gene expression in normal cells epigenetic modifications work in concert with genetic mechanisms. In contrast to genetic mutations, epigenetics encompasses the wide range of heritable changes in gene expression that do not result from alteration in the DNA sequence itself. A dysregulation of epigenetic modifications results in diseases such as cancer or autoimmune diseases. Since these epigenetic modifications of the DNA and the histones are reversible they are good targets for novel therapeutic intervention

Epigenetik in der Rheumatologie

Zusammenfassung: Die Erbsubstanz aller Lebewesen besteht aus DNA ("desoxyribonucleic acid"). Jede Zelle unseres Körpers enthält die gleiche genetische Ausstattung. In embryonalen Stammzellen ist eine gleichbleibende Anzahl Gene aktiv, und die Zellen sind identisch in ihrem Aufbau und ihrer Funktion. Sobald sich aber unterschiedlich spezialisierte Zellen entwickeln (Differenzierung), unterscheiden sie sich deutlich voneinander, wie z.B. Leber- von den Nervenzellen. Diese Unterschiede gehen nicht auf Änderungen in der Sequenz der DNA zurück, sondern darauf, dass in verschiedenen Zellen unterschiedliche Gene aktiv sind. Das bedeutet, dass ganz gezielt Informationen in der einen Zelle unterdrückt werden müssen, die in anderen wiederum aktiv sind und so verhindert wird, dass z.B. Muskelzellen Haare hervorbringen oder Gehirnzellen Leberenzyme produzieren. Wie kommt es, dass Gene in differenzierten Zellen ein gewebetypisches Set an Genen aktivieren, während sie in anderen Zellen abgeschaltet sind

Publication of original research in urologic journals - a neglected orphan?

The pathophysiologic mechanisms behind urologic disease are increasingly being elucidated. The object of this investigation was to evaluate the publication policies of urologic journals during a period of progressively better understanding and management of urologic disease. Based on the ISI Web of Knowledge Journal Citation Reports and the PubMed database, the number and percentage of original experimental, original clinical, review or commentarial articles published between 2002–2010 in six leading urologic journals were analyzed. “British Journal of Urology International”, “European Urology”, “Urologic Oncology-Seminars and Original Investigations” (“Urologic Oncology”), “Urology”, “The Journal of Urology”, and “World Journal of Urology” were chosen, because these journals publish articles in all four categories. The publication policies of the six journals were very heterogeneous during the time period from 2002 to 2010. The percentage of original experimental and original clinical articles, related to all categories, remained the same in “British Journal of Urology International”, “Urologic Oncology”, “Urology” and “The Journal of Urology”. The percentage of experimental reports in “World Journal of Urology” between 2002–2010 significantly increased from 10 to 20%. A distinct elevation in the percentage of commentarial articles accompanied by a reduction of clinical articles became evident in “European Urology” which significantly correlated with a large increase in the journal’s impact factor. No clearly superior policy could be identified with regard to a general increase in the impact factors from all the journals. The publication policy of urologic journals does not expressly reflect the increase in scientific knowledge, which has occurred over the period 2002–2010. One way of increasing the exposure of urologists to research and expand the interface between experimental and clinical research, would be to enlarge the percentage of experimental articles published. There is no indication that such policy would be detrimental to a journal’s impact factor

Resistance after chronic application of the HDAC-inhibitor valproic acid is associated with elevated Akt activation in renal cell carcinoma in vivo

Targeted drugs have significantly improved the therapeutic options for advanced renal cell carcinoma (RCC). However, resistance often develops, negating the benefit of these agents. In the present study, the molecular mechanisms of acquired resistance towards the histone deacetylase (HDAC) inhibitor valproic acid (VPA) in a RCC in vivo model were investigated. NMRI:nu/nu mice were transplanted with Caki-1 RCC cells and then treated with VPA (200 mg/kg/day). Controls remained untreated. Based on tumor growth dynamics, the mice were divided into “responders” and “non-responders” to VPA. Histone H3 and H4 acetylation and expression of cell signaling and cell cycle regulating proteins in the RCC mouse tumors were evaluated by Western blotting. Tumor growth of VPA responders was significantly diminished, whereas that of VPA non-responders even exceeded control values. Cdk1, 2 and 4 proteins were strongly enhanced in the non-responders. Importantly, Akt expression and activity were massively up-regulated in the tumors of the VPA non-responders. Chronic application (12 weeks) of VPA to Caki-1 cells in vitro evoked a distinct elevation of Akt activity and cancer cells no longer responded with cell growth reduction, compared to the short 2 week treatment. We assume that chronic use of an HDAC-inhibitor is associated with (re)-activation of Akt, which may be involved in resistance development. Consequently, combined blockade of both HDAC and Akt may delay or prevent drug resistance in RCC

On a quasilinear degenerated system arising in semiconductors theory

A drift-diffusion model for semiconductors with nonlinear diffusion is considered. The model consists of two quasilinear degenerated parabolic equations for the carrier densities and the Poisson equation for the electric potential. We also assume Lipschitz continuous non linearities in the drift and {em generation-recombination terms. Existence of weak solutions is proven by using a regularization technique. Uniqueness of solutions is proven when either the diffusion term $varphi$ is strictly increasing and solutions have spatial derivatives in $L^1(Q_T)$ or when $varphi$ is non decreasing and a suitable entropy condition is fullfilled by the electric potential