Quasi-particle Lifetimes in a d_{x^2-y^2} Superconductor

We consider the lifetime of quasi-particles in a d-wave superconductor due to scattering from antiferromagnetic spin-fluctuations, and explicitly separate the contribution from Umklapp processes which determines the electrical conductivity. Results for the temperature dependence of the total scattering rate and the Umklapp scattering rate are compared with relaxation rates obtained from thermal and microwave conductivity measurements, respectively.Comment: 14 pages, 4 figure

Instability of charge ordered states in doped antiferromagnets

We analyze the induced interactions between localized holes in weakly-doped Heisenberg antiferromagnets due to the modification of the quantum zero point spin wave energy; i.e. the analogue of the Casimir effect. We show that this interaction is uniformly attractive and falls off as r^{-2 d+1} in d dimensions. For ``stripes'', i.e parallel (d-1)-dimensional hypersurfaces of localized holes, the interaction energy per unit hyperarea is attractive and falls, generically, like r^{-d}. We argue that, in the absence of a long-range Coulomb repulsion between holes, this interaction leads to an instability of any charge-ordered state in the dilute doping limit.Comment: Revtex, 5 pages two-column format, 3 ps figures (epsf). Two references added and some textual change

Comparative analysis of cell death induction by Taurolidine in different malignant human cancer cell lines

<p>Abstract</p> <p>Background</p> <p>Taurolidine (TRD) represents an anti-infective substance with anti-neoplastic activity in many malignant cell lines. So far, the knowledge about the cell death inducing mechanisms and pathways activated by TRD is limited. The aim of this study was therefore, to perform a comparative analysis of cell death induction by TRD simultaneously in different malignant cell lines.</p> <p>Materials and methods</p> <p>Five different malignant cell lines (HT29/Colon, Chang Liver/Liver, HT1080/fibrosarcoma, AsPC-1/pancreas and BxPC-3/pancreas) were incubated with increasing concentrations of TRD (100 μM, 250 μM and 1000 μM) for 6 h and 24 h. Cell viability, apoptosis and necrosis were analyzed by FACS analysis (Propidiumiodide/AnnexinV staining). Additionally, cells were co-incubated with the caspase Inhibitor z-VAD, the radical scavenger N-Acetylcystein (NAC) and the Gluthation depleting agent BSO to examine the contribution of caspase activation and reactive oxygen species in TRD induced cell death.</p> <p>Results</p> <p>All cell lines were susceptible to TRD induced cell death without resistance toward this anti-neoplastic agent. However, the dose response effects were varying largely between different cell lines. The effect of NAC and BSO co-treatment were highly different among cell lines - suggesting a cell line specific involvement of ROS in TRD induced cell death. Furthermore, impact of z-VAD mediated inhibition of caspases was differing strongly among the cell lines.</p> <p>Conclusion</p> <p>This is the first study providing a simultaneous evaluation of the anti-neoplastic action of TRD across several malignant cell lines. The involvement of ROS and caspase activation was highly variable among the five cell lines, although all were susceptible to TRD induced cell death. Our results indicate, that TRD is likely to provide multifaceted cell death mechanisms leading to a cell line specific diversity.</p

TRAIL and Taurolidine induce apoptosis and decrease proliferation in human fibrosarcoma

<p>Abstract</p> <p>Background</p> <p>Disseminated soft tissue sarcoma still represents a therapeutic dilemma because effective cytostatics are missing. Therefore we tested TRAIL and Tarolidine (TRD), two substances with apoptogenic properties on human fibrosarcoma (HT1080).</p> <p>Methods</p> <p>Viability, apoptosis and necrosis were visualized by TUNEL-Assay and quantitated by FACS analysis (Propidiumiodide/AnnexinV staining). Gene expression was analysed by RNA-Microarray and the results validated for selected genes by rtPCR. Protein level changes were documented by Western Blot analysis. NFKB activity was analysed by ELISA and proliferation assays (BrdU) were performed.</p> <p>Results and discussion</p> <p>The single substances TRAIL and TRD induced apoptotic cell death and decreased proliferation in HT1080 cells significantly. Gene expression of several genes related to apoptotic pathways (TRAIL: <it>ARHGDIA</it>, <it>NFKBIA</it>, <it>TNFAIP3</it>; TRD: <it>HSPA1A/B</it>, <it>NFKBIA</it>, <it>GADD45A</it>, <it>SGK</it>, <it>JUN</it>, <it>MAP3K14</it>) was changed. The combination of TRD and TRAIL significantly increased apoptotic cell death compared to the single substances and lead to expression changes in a variety of genes (<it>HSPA1A/B</it>, <it>NFKBIA</it>, <it>PPP1R15A</it>, <it>GADD45A</it>, <it>AXL</it>, <it>SGK</it>, <it>DUSP1</it>, <it>JUN</it>, <it>IRF1</it>, <it>MYC</it>, <it>BAG5</it>, <it>BIRC3</it>). NFKB activity assay revealed an antipodal regulation of the several subunits of NFKB by TRD and TRD+TRAIL compared to TRAIL alone.</p> <p>Conclusion</p> <p>TRD and TRAIL are effective to induce apoptosis and decrease proliferation in human fibrosarcoma. A variety of genes seems to be involved, pointing to the NFKB pathway as key regulator in TRD/TRAIL-mediated apoptosis.</p

Influence of next-nearest-neighbor electron hopping on the static and dynamical properties of the 2D Hubbard model

Comparing experimental data for high temperature cuprate superconductors with numerical results for electronic models, it is becoming apparent that a hopping along the plaquette diagonals has to be included to obtain a quantitative agreement. According to recent estimations the value of the diagonal hopping $t'$ appears to be material dependent. However, the values for $t'$ discussed in the literature were obtained comparing theoretical results in the weak coupling limit with experimental photoemission data and band structure calculations. The goal of this paper is to study how $t'$ gets renormalized as the interaction between electrons, $U$, increases. For this purpose, the effect of adding a bare diagonal hopping $t'$ to the fully interacting two dimensional Hubbard model Hamiltonian is investigated using numerical techniques. Positive and negative values of $t'$ are analyzed. Spin-spin correlations, $n(\bf{k})$, $\langle n\rangle$ vs $\mu$, and local magnetic moments are studied for values of $U/t$ ranging from 0 to 6, and as a function of the electronic density. The influence of the diagonal hopping in the spectral function $A(\bf{k},\omega)$ is also discussed, and the changes in the gap present in the density of states at half-filling are studied. We introduce a new criterion to determine probable locations of Fermi surfaces at zero temperature from $n(\bf{k})$ data obtained at finite temperature. It appears that hole pockets at ${\bf{k}}=(\pi/2,\pi/2)$ may be induced for negative $t'$ while a positive $t'$ produces similar features at ${\bf{k}}=(\pi,0)$ and $(0,\pi)$. Comparisons with the standard 2D Hubbard ($t'=0$) model indicate that a negative $t'$ hopping amplitude appears to be dynamically generated. In general, we conclude that it is very dangerous to extract a bare parameter of the Hamiltonian $(t')$ from PES data whereComment: 9 pages (RevTex 3.0), 12 figures (postscript), files packed with uufile

Hole Doping Evolution of the Quasiparticle Band in Models of Strongly Correlated Electrons for the High-T_c Cuprates

Quantum Monte Carlo (QMC) and Maximum Entropy (ME) techniques are used to study the spectral function $A({\bf p},\omega)$ of the one band Hubbard model in strong coupling including a next-nearest-neighbor electronic hopping with amplitude $t'/t= -0.35$. These values of parameters are chosen to improve the comparison of the Hubbard model with angle-resolved photoemission (ARPES) data for $Sr_2 Cu O_2 Cl_2$. A narrow quasiparticle (q.p.) band is observed in the QMC analysis at the temperature of the simulation $T=t/3$, both at and away from half-filling. Such a narrow band produces a large accumulation of weight in the density of states at the top of the valence band. As the electronic density $$ decreases further away from half-filling, the chemical potential travels through this energy window with a large number of states, and by $\sim 0.70$ it has crossed it entirely. The region near momentum $(0,\pi)$ and $(\pi,0)$ in the spectral function is more sensitive to doping than momenta along the diagonal from $(0,0)$ to $(\pi,\pi)$. The evolution with hole density of the quasiparticle dispersion contains some of the features observed in recent ARPES data in the underdoped regime. For sufficiently large hole densities the ``flat'' bands at $(\pi,0)$ cross the Fermi energy, a prediction that could be tested with ARPES techniques applied to overdoped cuprates. The population of the q.p. band introduces a {\it hidden} density in the system which produces interesting consequences when the quasiparticles are assumed to interact through antiferromagnetic fluctuations and studied with the BCS gap equation formalism. In particular, a region of extended s-wave is found to compete with d-wave in the overdoped regime, i.e. when the chemical potential has almost entirely crossed the q.p.Comment: 14 pages, Revtex, with 13 embedded ps figures, submitted to Phys. Rev. B., minor modifications in the text and in figures 1b, 2b, 3b, 4b, and 6

Nitric oxide sensing in plants is mediated by proteolytic control of group VII ERF transcription factors

Nitric oxide (NO) is an important signaling compound in prokaryotes and eukaryotes. In plants, NO regulates critical developmental transitions and stress responses. Here, we identify a mechanism for NO sensing that coordinates responses throughout development based on targeted degradation of plant-specific transcriptional regulators, the group VII ethylene response factors (ERFs). We show that the N-end rule pathway of targeted proteolysis targets these proteins for destruction in the presence of NO, and we establish them as critical regulators of diverse NO-regulated processes, including seed germination, stomatal closure, and hypocotyl elongation. Furthermore, we define the molecular mechanism for NO control of germination and crosstalk with abscisic acid (ABA) signaling through ERF-regulated expression of ABSCISIC ACID INSENSITIVE5 (ABI5). Our work demonstrates how NO sensing is integrated across multiple physiological processes by direct modulation of transcription factor stability and identifies group VII ERFs as central hubs for the perception of gaseous signals in plants

A defensive strategy against beam training attack in 5G mmWave networks for manufacturing

Millimeter-wave (mmWave) carriers are an essential building block of fifth-generation (5G) systems. Satisfactory performance of the communications over the mmWave spectrum requires an alignment between the signal beam of the transmitter and receiver, achieved via beam training protocols. Nevertheless, beam training is vulnerable to jamming attacks, where the attacker intends to send jamming signals over different spatial directions to confuse legitimate nodes. This paper focuses on defending against this attack in smart factories where a moving Automated Guided Vehicle (AGV) communicates with a base station via a mmWave carrier. We introduce a defensive strategy to cope with jamming attacks, including two stages: jamming detection and jamming mitigation. Developed based on autoencoders, both algorithms can learn the characteristics/features of the received signals at the AGV. They can be employed consecutively before performing the downlink data transmission. In particular, once a jamming attack is identified, the jamming mitigation can be utilized to retrieve the corrupted received signal strength vector, allowing a better decision during the beam training operation. In addition, the proposed algorithm is straightforward and fully compliant with the existing beam training protocols in 5G New Radio. The numerical results show that not only the proposed defensive strategy can capture more than 80% of attack events, but it also improves the average signal-to-interference-plus-noise-ratio significantly, i.e., up to 15 dB

Sub-6 GHz channel modelling and evaluation in indoor industrial environments

This paper presents sub-6 GHz channel measurements using a directional antenna at the transmitter and a directional or omnidirectional antenna at the receiver at 4.145 GHz in sparse and dense industrial environments for a line-of-sight scenario. Furthermore, the first measured over-the-air error vector magnitude (EVM) results depending on different 5G new radio modulation and coding schemes (MCSs of16 QAM, 64 QAM and 256 QAM) are provided. From the measurement campaigns, the path loss exponents (PLE) using a directional and an omnidirectional antenna at the receiver in the sparse and the dense environment are 1.24/1.39 and 1.35/1.5, respectively. PLE results are lower than the theoretical free space PLE of 2, indicating that indoor industrial environments have rich multipaths. The measured power delay profiles show the maximum root mean square (RMS) delay spreads of 11 ns with a directional antenna and 34 ns with an omnidirectional antenna at the receiver in a sparse industrial environment. However, in a dense industrial environment the maximum RMS delay spreads are significantly increased: maximum RMS delay spreads range from 226 to 282 ns for the omnidirectional and the directional antenna configuration. EVM measurements show that to increase coverage and enable higher MCS modes to be used for reliable data transmission, in both industrial environments using a directional antenna at the transmitter and the receiver is required. The large-scale path loss models, multipath time dispersion characteristics and EVM results provide insight into the deployments of 5G networks operating at sub-6 GHz frequency bands in different industrial environments

The CYP2J2 G-50T polymorphism and myocardial infarction in patients with cardiovascular risk profile

<p>Abstract</p> <p>Background</p> <p>Cytochrome P450 (CYP) enzyme 2J2, an epoxygenase predominantly expressed in the heart, metabolises arachidonic acid to biologically active eicosanoids. One of the CYP2J2 products, 11, 12-epoxyeicosatrienoic acid, has several vasoprotective effects. The CYP2J2-G-50T-promotor polymorphism decreases gene expression and is associated with coronary artery disease. This association supports the vascular protective role of CYP-derived eicosanoids in cardiovascular disease. In the present study, we investigated the influence of this polymorphism on survived myocardial infarction in two study groups of patients with on average high cardiovascular risk profile.</p> <p>Methods</p> <p>The CYP2J2 polymorphism was genotyped in two groups of patients that were collected with the same method of clinical data collection. Data from 512 patients with sleep apnoea (group: OSA) and on average high cardiovascular risk profile and from another 488 patients who were admitted for coronary angiography (CAR-group) were evaluated for a potential correlation of the CYP2J2 polymorphism G-50T and a history of myocardial infarction. The G-50T polymorphism of the CYP2J2 gene was genotyped by allele specific restriction and light cycler analysis.</p> <p>Results</p> <p>The T-allele of the polymorphism was found in 111 (11.1%; CAR-group: N = 65, 13.3%; OSA: N = 46, 9.0%). 146 patients had a history of myocardial infarction (CAR: N = 120, 24.6%; OSA: N = 26, 5.1%). Cardiovascular risk factors were equally distributed between the different genotypes of the CYP2J2 G-50T polymorphism. In the total group of 1000 individuals, carriers of the T-allele had significantly more myocardial infarctions compared to carriers of the wild type (T/T or G/T: 21.6%; G/G: 13.7%; p = 0.026, odds ratio 1.73, 95%-CI [1.06–2.83]). In the multivariate logistic regression analysis the odds ratio for a history of myocardial infarction in carriers of the T-allele was 1.611, 95%-CI [0.957–2.731] but this trend was not significant (p = 0.073).</p> <p>Conclusion</p> <p>In presence of other risk factors, the CYP2J2 G-50T failed to show a significant role in the development of myocardial infarction. However, since our result is close to the border of significance, this question should be clarified in larger, prospective studies in the future.</p