Quantum theory of the charge stability diagram of semiconductor double quantum dot systems

We complete our recently introduced theoretical framework treating the double quantum dot system with a generalized form of Hubbard model. The effects of all quantum parameters involved in our model on the charge stability diagram are discussed in detail. A general formulation of the microscopic theory is presented, and truncating at one orbital per site, we study the implication of different choices of the model confinement potential on the Hubbard parameters as well as the charge stability diagram. We calculate the charge stability diagram keeping three orbitals per site and find that the effect of additional higher-lying orbitals on the subspace with lowest-energy orbitals only can be regarded as a small renormalization of Hubbard parameters, thereby justifying our practice of keeping only the lowest-orbital in all other calculations. The role of the harmonic oscillator frequency in the implementation of the Gaussian model potential is discussed, and the effect of an external magnetic field is identified to be similar to choosing a more localized electron wave function in microscopic calculations. The full matrix form of the Hamiltonian including all possible exchange terms, and several peculiar charge stability diagrams due to unphysical parameters are presented in the appendix, thus emphasizing the critical importance of a reliable microscopic model in obtaining the system parameters defining the Hamiltonian.Comment: 19 pages, 15 figure

Suppression of high pTp_T hadron spectra in p+Ap+A collisions

Multiple hard and semi-hard parton scatterings in high-energy $p+A$ collisions involve multi-parton correlation in both momentum and flavor inside the projectile proton which will lead to modification of the final hadron spectra relative to that in $p+p$ collisions. Such modification of final hadron transverse momentum spectra in $p+A$ collisions is studied within HIJING 2.1 Monte Carlo model which includes nuclear shadowing of the initial parton distributions and transverse momentum broadening. Multi-parton flavor and momentum correlation inside the projectile are incorporated through flavor and momentum conservation which are shown to modify the flavor content and momentum spectra of final partons and most importantly lead to suppression of large $p_{T}$ hadron spectra in $p+A$ collisions at both RHIC and LHC energies.Comment: 4 pages, 3 figures, talk given at the 5th international conference on Hard and Electromagnetic Probes of High Energy nuclear Collisions (Hard Probes 2012

Deciphering cancer heterogeneity: the biological space

Most lethal solid tumors including hepatocellular carcinoma (HCC) are considered incurable due to extensive heterogeneity in clinical presentation and tumor biology. Tumor heterogeneity may result from different cells of origin, patient ethnicity, etiology, underlying disease and diversity of genomic and epigenomic changes which drive tumor development. Cancer genomic heterogeneity thereby impedes treatment options and poses a significant challenge to cancer management. Studies of the HCC genome have revealed that although various genomic signatures identified in different HCC subgroups share a common prognosis, each carries unique molecular changes which are linked to different sets of cancer hallmarks whose misregulation has been proposed by Hanahan and Weinberg to be essential for tumorigenesis. We hypothesize that these specific sets of cancer hallmarks collectively occupy different tumor biological space representing the misregulation of different biological processes. In principle, a combination of different cancer hallmarks can result in new convergent molecular networks that are unique to each tumor subgroup and represent ideal druggable targets. Due to the ability of the tumor to adapt to external factors such as treatment or changes in the tumor microenvironment, the tumor biological space is elastic. Our ability to identify distinct groups of cancer patients with similar tumor biology who are most likely to respond to a specific therapy would have a significant impact on improving patient outcome. It is currently a challenge to identify a particular hallmark or a newly emerged convergent molecular network for a particular tumor. Thus, it is anticipated that the integration of multiple levels of data such as genomic mutations, somatic copy number aberration, gene expression, proteomics, and metabolomics, may help us grasp the tumor biological space occupied by each individual, leading to improved therapeutic intervention and outcome

The clinical potential of microRNAs

MicroRNAs are small noncoding RNAs that function to control gene expression. These small RNAs have been shown to contribute to the control of cell growth, differentiation and apoptosis, important features related to cancer development and progression. In fact, recent studies have shown the utility of microRNAs as cancer-related biomarkers. This is due to the finding that microRNAs display altered expression profiles in cancers versus normal tissue. In addition, microRNAs have been associated with cancer progression. In this review, the mechanisms to alter microRNA expression and their relation to cancer will be addressed. Moreover, the potential application of microRNAs in clinical settings will also be highlighted. Finally, the challenges regarding the translation of research involving microRNAs to the clinical realm will be discussed

Wnt/beta-catenin signaling activates microRNA-181 expression in hepatocellular carcinoma

<p>Abstract</p> <p>Background</p> <p>Hepatocellular carcinoma (HCC) is a malignant cancer with an observable heterogeneity and microRNAs are functionally associated with the tumorigenesis of HCC. We recently identified that EpCAM (CD326)-positive cells isolated from alpha-fetoprotein (AFP)-positive HCC samples are hepatic cancer stem cells (HepCSCs). EpCAM⁺AFP⁺HepCSCs have an activated Wnt/β-catenin signaling with a parallel increased expression of all four microRNA-181 family members. We hypothesized that Wnt/β-catenin signaling transcriptionally activates microRNA-181s in HCC.</p> <p>Results</p> <p>Using both western blot and quantitative reverse transcriptase-PCR analyses, we found that the expression of all four microRNA-181 family members was positively correlated with β-catenin expression in HCC cell lines. MicroRNA-181 expression could be directly induced upon an activation of Wnt/β-catenin signaling, which includes Wnt10B overexpression, inhibition of GSK3β signaling by LiCl, or forced expression of β-catenin/Tcf4. Moreover, microRNA-181 expression was inhibited upon an inactivation of Wnt/β-catenin signaling by an induction of adenomatosis polyposis coli (APC) expression or silencing β-catenin via RNA interference. In addition, seven putative β-catenin/Tcf4 binding sites were identified in the promoter region of the microRNA-181a-2 and microRNA-181b-2 transcripts. Consistently, we found that Tcf4 interacted with these regions <it>in vivo </it>using chromatin immunoprecipitation assay.</p> <p>Conclusions</p> <p>Taken together, our results demonstrate that microRNA-181s are transcriptionally activated by the Wnt/beta-catenin signaling pathway in HCC.</p

Retinal oscillations carry visual information to cortex

Thalamic relay cells fire action potentials that transmit information from retina to cortex. The amount of information that spike trains encode is usually estimated from the precision of spike timing with respect to the stimulus. Sensory input, however, is only one factor that influences neural activity. For example, intrinsic dynamics, such as oscillations of networks of neurons, also modulate firing pattern. Here, we asked if retinal oscillations might help to convey information to neurons downstream. Specifically, we made whole-cell recordings from relay cells to reveal retinal inputs (EPSPs) and thalamic outputs (spikes) and analyzed these events with information theory. Our results show that thalamic spike trains operate as two multiplexed channels. One channel, which occupies a low frequency band (<30 Hz), is encoded by average firing rate with respect to the stimulus and carries information about local changes in the image over time. The other operates in the gamma frequency band (40-80 Hz) and is encoded by spike time relative to the retinal oscillations. Because these oscillations involve extensive areas of the retina, it is likely that the second channel transmits information about global features of the visual scene. At times, the second channel conveyed even more information than the first.Comment: 21 pages, 10 figures, submitted to Frontiers in Systems Neuroscienc

Attosecond Precision Multi-km Laser-Microwave Network

Synchronous laser-microwave networks delivering attosecond timing precision are highly desirable in many advanced applications, such as geodesy, very-long-baseline interferometry, high-precision navigation and multi-telescope arrays. In particular, rapidly expanding photon science facilities like X-ray free-electron lasers and intense laser beamlines require system-wide attosecond-level synchronization of dozens of optical and microwave signals up to kilometer distances. Once equipped with such precision, these facilities will initiate radically new science by shedding light on molecular and atomic processes happening on the attosecond timescale, such as intramolecular charge transfer, Auger processes and their impact on X-ray imaging. Here, we present for the first time a complete synchronous laser-microwave network with attosecond precision, which is achieved through new metrological devices and careful balancing of fiber nonlinearities and fundamental noise contributions. We demonstrate timing stabilization of a 4.7-km fiber network and remote optical-optical synchronization across a 3.5-km fiber link with an overall timing jitter of 580 and 680 attoseconds RMS, respectively, for over 40 hours. Ultimately we realize a complete laser-microwave network with 950-attosecond timing jitter for 18 hours. This work can enable next-generation attosecond photon-science facilities to revolutionize many research fields from structural biology to material science and chemistry to fundamental physics.Comment: 42 pages, 13 figure