On The Violation Of Marshall-Peierls Sign Rule In The Frustrated J1−J2J_{1}-J_{2} Heisenberg Antiferromagnet

We present a number of arguments in favor of the suggestion that the Marshall-Peierls sign rule survives the frustration in the square-lattice Heisenberg antiferromagnet with frustrating next-nearest-neighbor (diagonal) bonds ($J_{1}-J_{2}$ model) for relatively large values of the parameter $J_{2}/J_{1}$. Both the spin-wave analysis and the exact-diagonalization data concerning the weight of Marshall states support the above suggestion.Comment: 8 pages, LaTex, 2 figurs on reques

Y-Scaling Analysis of the Deuteron Within the Light-Front Dynamics Method

The concept of relativistic scaling is applied to describe the most recent data from inclusive electron-deuteron scattering at large momentum transfer. We calculate the asymptotic scaling function f(y) of the deuteron using its relationship with the nucleon momentum distribution. The latter is obtained in the framework of the relativistic light-front dynamics (LFD) method, in which the deuteron is described by six invariant functions f_{i} (i=1,...,6) instead of two (S and D waves) in the nonrelativistic case. Comparison of the LFD asymptotic scaling function with other calculations using $S$ and $D$ waves corresponding to various nucleon-nucleon potentials, as well as with the Bethe-Salpeter result is made. It is shown that for |y|> 400 MeV/c the differences between the LFD and the nonrelativistic scaling functions become larger.Comment: 7 pages, 5 figures, Talk at 21-st International Workshop on Nuclear Theory, Rila Mountains, Bulgaria, June 10-15, 200

Solution of the Riemann problem for polarization waves in a two-component Bose-Einstein condensate

We provide a classification of the possible flow of two-component Bose-Einstein condensates evolving from initially discontinuous profiles. We consider the situation where the dynamics can be reduced to the consideration of a single polarization mode (also denoted as "magnetic excitation") obeying a system of equations equivalent to the Landau-Lifshitz equation for an easy-plane ferro-magnet. We present the full set of one-phase periodic solutions. The corresponding Whitham modulation equations are obtained together with formulas connecting their solutions with the Riemann invariants of the modulation equations. The problem is not genuinely nonlinear, and this results in a non-single-valued mapping of the solutions of the Whitham equations with physical wave patterns as well as to the appearance of new elements --- contact dispersive shock waves --- that are absent in more standard, genuinely nonlinear situations. Our analytic results are confirmed by numerical simulations

Analytical representation of elastic scattering cross sections of low energy electrons by atmospheric gases

Analytical representations of the elastic scattering cross sections of electrons with energies of 0.01-1 keV in atmospheric gases of N2, O2, O are given. These representations are suitable for the Monte Carlo method

Arsenite Sensitizes Human Melanomas to Apoptosis via Tumor Necrosis Factor α-Mediated Pathway

Arsenic is a well established human carcinogen and is associated with a variety of cancers including those of the skin. Paradoxically, arsenic has also been used, amid at low doses, in the treatment of leukemia for over a century. Here we demonstrate that low to moderate concentrations of arsenite (2-10 μm) that has little or no effect on normal melanocytes may induce apoptosis of human melanomas including highly metastatic ones despite their low surface Fas levels. The two prerequisites that dictate apoptotic response of melanomas upon arsenite treatment are low nuclear NF-κB activity and an endogenous expression of tumor necrosis factor α. Under these conditions, melanoma cells acquired sensitivity to tumor necrosis factor α-mediated killing. On the other hand, signaling pathways including those of phosphatidylinositol 3-kinase-AKT, MEK-ERK, and JNK play a protective role against arsenite-induced oxidative stress and apoptosis in melanoma cells. Suppression of these pathways dramatically accelerates arsenite-induced apoptosis. Taken together, these data could provide potential approaches to sensitize melanomas to the cytotoxic effects of arsenite through modulating the signaling pathways

Radiation-Induced Glioblastoma Signaling Cascade Regulates Viability, Apoptosis and Differentiation of Neural Stem Cells (NSC)

Ionizing radiation alone or in combination with chemotherapy is the main treatment modality for brain tumors including glioblastoma. Adult neurons and astrocytes demonstrate substantial radioresistance; in contrast, human neural stem cells (NSC) are highly sensitive to radiation via induction of apoptosis. Irradiation of tumor cells has the potential risk of affecting the viability and function of NSC. In this study, we have evaluated the effects of irradiated glioblastoma cells on viability, proliferation and differentiation potential of non-irradiated (bystander) NSC through radiation-induced signaling cascades. Using media transfer experiments, we demonstrated significant effects of the U87MG glioblastoma secretome after gamma-irradiation on apoptosis in non-irradiated NSC. Addition of anti-TRAIL antibody to the transferred media partially suppressed apoptosis in NSC. Furthermore, we observed a dramatic increase in the production and secretion of IL8, TGFβ1 and IL6 by irradiated glioblastoma cells, which could promote glioblastoma cell survival and modify the effects of death factors in bystander NSC. While differentiation of NSC into neurons and astrocytes occurred efficiently with the corresponding differentiation media, pretreatment of NSC for 8 h with medium from irradiated glioblastoma cells selectively suppressed the differentiation of NSC into neurons, but not into astrocytes. Exogenous IL8 and TGFβ1 increased NSC/NPC survival, but also suppressed neuronal differentiation. On the other hand, IL6 was known to positively affect survival and differentiation of astrocyte progenitors. We established a U87MG neurosphere culture that was substantially enriched by SOX2+ and CD133+ glioma stem-like cells (GSC). Gamma-irradiation up-regulated apoptotic death in GSC via the FasL/Fas pathway. Media transfer experiments from irradiated GSC to non-targeted NSC again demonstrated induction of apoptosis and suppression of neuronal differentiation of NSC. In summary, intercellular communication between glioblastoma cells and bystander NSC/NPC could be involved in the amplification of cancer pathology in the brain

Induction of Apoptotic Death and Retardation of Neuronal Differentiation of Human Neural Stem Cells by Sodium Arsenite Treatment

Chronic arsenic toxicity is a global health problem that affects more than 100 million people worldwide. Long-term health effects of inorganic sodium arsenite in drinking water may result in skin, lung and liver cancers and in severe neurological abnormalities. We investigated in the present study whether sodium arsenite affects signaling pathways that control cell survival, proliferation and neuronal differentiation of human neural stem cells (NSC). We demonstrated that the critical signaling pathway, which was suppressed by sodium arsenite in NSC, was the protective PI3K–AKT pathway. Sodium arsenite (2–4 μM) also caused down-regulation of Nanog, one of the key transcription factors that control pluripotency and self-renewal of stem cells. Mitochondrial damage and cytochrome-c release induced by sodium arsenite exposure was followed by initiation of the mitochondrial apoptotic pathway in NSC. Beside caspase-9 and caspase-3 inhibitors, suppression of JNK activity decreased levels of arsenite-induced apoptosis in NSC. Neuronal differentiation of NSC was substantially inhibited by sodium arsenite exposure. Overactivation of JNK1 and ERK1/2 and down-regulation of PI3K–AKT activity induced by sodium arsenite were critical factors that strongly affected neuronal differentiation. In conclusion, sodium arsenite exposure of human NSC induces the mitochondrial apoptotic pathway, which is substantially accelerated due to the simultaneous suppression of PI3K–AKT. Sodium arsenite also negatively affects neuronal differentiation of NSC through overactivation of MEK–ERK and suppression of PI3K–AKT