Nature of the many-body excitations in a quantum wire: Theory and experiment

The natural excitations of an interacting one-dimensional system at low energy are hydrodynamic modes of Luttinger liquid, protected by the Lorentz invariance of the linear dispersion. We show that beyond low energies, where quadratic dispersion reduces the symmetry to Galilean, the main character of the many-body excitations changes into a hierarchy: calculations of dynamic correlation functions for fermions (without spin) show that the spectral weights of the excitations are proportional to powers of $\mathcal{R}^{2}/L^{2}$, where $\mathcal{R}$ is a length-scale related to interactions and $L$ is the system length. Thus only small numbers of excitations carry the principal spectral power in representative regions on the energy-momentum planes. We have analysed the spectral function in detail and have shown that the first-level (strongest) excitations form a mode with parabolic dispersion, like that of a renormalised single particle. The second-level excitations produce a singular power-law line shape to the first-level mode and multiple power-laws at the spectral edge. We have illustrated crossover to Luttinger liquid at low energy by calculating the local density of state through all energy scales: from linear to non-linear, and to above the chemical potential energies. In order to test this model, we have carried out experiments to measure momentum-resolved tunnelling of electrons (fermions with spin) from/to a wire formed within a GaAs heterostructure. We observe well-resolved spin-charge separation at low energy with appreciable interaction strength and only a parabolic dispersion of the first-level mode at higher energies. We find structure resembling the second-level excitations, which dies away rapidly at high momentum in line with the theoretical predictions here.We acknowledge financial support from the UK EPSRC through Grants No. EP/J01690X/1 and No. EP/J016888/1 and from the DFG through SFB/TRR 49. This research was supported in part by the National Science Foundation under Grant No. NSF PHY11-25915.This is the author accepted manuscript. The final version is available from APS via http://dx.doi.org/10.1103/PhysRevB.93.07514

Estimation of Biomass Heat Storage Using Thermal Infrared Imagery: Application to a Walnut Orchard

A new method to estimate tree biomass heat storage from thermal infrared (TIR) imaging of biomass surface temperature is presented. TIR images of the canopy are classified into trunk, branches, and leaves. The one-dimensional heat equation in cylindrical coordinates is forced with trunk and branch surface temperatures to simulate the temperature distribution and heat storage in tree trunks and branches. Assuming uniform leaf temperatures, heat storage in leaves is computed from the surface temperature of the leaves separately for the sunlit upper and shaded lower canopy. The sum of trunk, branches, leaf, and air heat storage gives the canopy heat storage. Measurements in a walnut orchard near Davis, California, in early June 2007 showed that biomass heat storage was of the same order as air heat storage and about 1% of daytime and 9% of nighttime net radiation

Performance of mitochondrial DNA mutations detecting early stage cancer

<p>Abstract</p> <p>Background</p> <p>Mutations in the mitochondrial genome (mtgenome) have been associated with cancer and many other disorders. These mutations can be point mutations or deletions, or admixtures (heteroplasmy). The detection of mtDNA mutations in body fluids using resequencing microarrays, which are more sensitive than other sequencing methods, could provide a strategy to measure mutation loads in remote anatomical sites.</p> <p>Methods</p> <p>We determined the mtDNA mutation load in the entire mitochondrial genome of 26 individuals with different early stage cancers (lung, bladder, kidney) and 12 heavy smokers without cancer. MtDNA was sequenced from three matched specimens (blood, tumor and body fluid) from each cancer patient and two matched specimens (blood and sputum) from smokers without cancer. The inherited wildtype sequence in the blood was compared to the sequences present in the tumor and body fluid, detected using the Affymetrix Genechip^®Human Mitochondrial Resequencing Array 1.0 and supplemented by capillary sequencing for noncoding region.</p> <p>Results</p> <p>Using this high-throughput method, 75% of the tumors were found to contain mtDNA mutations, higher than in our previous studies, and 36% of the body fluids from these cancer patients contained mtDNA mutations. Most of the mutations detected were heteroplasmic. A statistically significantly higher heteroplasmy rate occurred in tumor specimens when compared to both body fluid of cancer patients and sputum of controls, and in patient blood compared to blood of controls. Only 2 of the 12 sputum specimens from heavy smokers without cancer (17%) contained mtDNA mutations. Although patient mutations were spread throughout the mtDNA genome in the lung, bladder and kidney series, a statistically significant elevation of tRNA and ND complex mutations was detected in tumors.</p> <p>Conclusion</p> <p>Our findings indicate comprehensive mtDNA resequencing can be a high-throughput tool for detecting mutations in clinical samples with potential applications for cancer detection, but it is unclear the biological relevance of these detected mitochondrial mutations. Whether the detection of tumor-specific mtDNA mutations in body fluidsy this method will be useful for diagnosis and monitoring applications requires further investigation.</p

ICB3E Induces INOS Expression by ROS-Dependent JNK and ERK Activation for Apoptosis of Leukemic Cells

The role of c-Jun N terminal Kinase (JNK) has been well documented in various cellular stresses where it leads to cell death. Similarly, extracellular signal-regulated kinase (ERK) which was identified as a signalling molecule for survival pathway has been shown recently to be involved in apoptosis also. Recently we reported that ICB3E, a synthetic analogue of Piper betle leaf-derived apoptosis-inducing agent hydroxychavicol (HCH), possesses anti-chronic myeloid leukemia (CML) acitivity in vitro and in vivo without insight on mechanism of action. Here we report that ICB3E is three to four times more potent than HCH in inducing apoptosis of leukemic cells without having appreciable effects on normal human peripheral blood mononuclear cells, mouse fibroblast cell line NIH3T3 and monkey kidney epithelial cell line Vero. ICB3E causes early accumulation of mitochondria-derived reactive oxygen species (ROS) in K562 cells. Unlike HCH, ICB3E treatment caused ROS dependent activation of both JNK, ERK and induced the expression of iNOS leading to generation of nitric oxide (NO). This causes cleavage of caspase 9, 3 and PARP leading to apoptosis. Lack of cleavage of caspase 8 and inability of blocking chimera antibody to DR5 or neutralizing antibody to Fas to reverse ICB3E-mediated apoptosis suggest the involvement of only intrinsic pathway. Our data reveal a novel ROS-dependent JNK/ERK-mediated iNOS activation pathway which leads to NO mediated cell death by ICB3