We discuss variationally optimized matrix-product states for the transverse-field Ising chain, using D × D matrices with small D ∈ {2 − 10}. For finite system size N there are energy minimums for symmetric as well as symmetry-broken states, which cross each other at a field value hc(N, D); thus the transition is first-order. A continuous transition develops as N → ∞. The asymptotic critical behavior is then always of mean-field type (the magnetization exponent β = 1/2), but a window of field strengths where true Ising scaling holds (β = 1/8) emerges with increasing D. We also demonstrate asymptotic mean-field behavior for infinite-size two-dimensional tensor-product (iPEPS) states with small tensors.PACS numbers: 75.10. Jm, 75.40.Mg, 75.40.Cx, 05.30.Rt Methods based on matrix-product states (MPSs) [1,2] have become the primary computational tools for studies of static as well as dynamic properties of one-dimensional quantum many-body systems [3]. Key steps in the development of these methods were White's density matrix renormalization group (DMRG) [4,5], the demonstration byÖstlund and Romer of its connection to MPSs [2], and later important insights from the field of quantum information theory. In particular, the concept of entanglement entropy (the area law) both explains the success of the approach in one dimension and its failure (violation of the area law) in higher dimensions [6][7][8]. The formulation of computational methods directly in terms of MPSs also led to a framework for efficient optimization of these states independently of the DMRG method [9][10][11], and to a long-sought way of computing time evolution [12]. The MPS approach also has a natural extension to higher dimensions which does obey the area law [7]-tensor-product states; also referred to as projected-entangled-pair-states (PEPSs) [13,14].In spite of numerous successful applications of MPSbased methods, some fundamental aspects of this class of quantum states have not yet been studied in detail. It is well known that the finite size D of the D × D matrices (the elements of which are the variational parameters) imposes a finite correlation length, and recently it has been recognized that scaling in D for infinite system size N can be carried out as an alternative to finite-size scaling [15] (i.e., D and N can be considered as different but equally valid ways to regularize the calculations). As in mean-field theory (which corresponds to D = 1), an MPS can break symmetries of the hamiltonian at a phase transition. Exactly how the critical behavior of the order parameter (the true scaling exponent β) emerges as a function of N and D has not been studied systematically, however. This may be partially due to technical challenges in properly optimizing an MPS close to a phase transition. Such issues are present also for the PEPS approach in two dimensions. Order-parameter curves often exhibit rounding [17], that may appear due to incomplete convergence, approximations made [15], or due to external fields included to stabilize the calculatio...

Development of nonimmunogenic and specific reporter genes to monitor gene expression in vivo is important for the optimization of gene therapy protocols. We developed a membrane-anchored form of mouse b-glucuronidase (mbG) as a reporter gene to hydrolyze a nonfluorescent glucuronide probe (fluorescein di-b-D-glucuronide, (FDGlcU) to a highly fluorescent reporter to assess the location and persistence of gene expression. A functional b-glucuronidase (bG) was stably expressed on the surface of murine CT26 colon adenocarcinoma cells where it selectively hydrolyzed the cell-impermeable FDGlcU probe. FDGlcU was also preferentially converted to fluorescent probe by (bG) on CT26 tumors. The fluorescent intensity in bG-expressing CT26 tumors was 240 times greater than the intensity in control tumors. Selective imaging of gene expression was also observed after intratumoral injection of adenoviral bG vector into carcinoma xenografts. Importantly, mbG did not induce an antibody response after hydrodynamic plasmid immunization of Balb/c mice, indicating that the reporter gene product displayed low immunogenicity. A membraneanchored form of human bG also allowed in vivo imaging, demonstrating that human bG can be employed for imaging. This imaging system therefore, displays good selectivity with low immunogenicity and may help assess the location, magnitude and duration of gene expression in living animals and humans.

Increasing the specificity of chemotherapy may improve the efficacy of cancer treatment. Toward this aim, we developed a strain of bacteria to express enzymes for selective prodrug activation and non-invasive imaging in tumors. b-glucuronidase and the luxCDABE gene cluster were expressed in the DH5a strain of Escherichia coli to generate DH5a-lux/bG. These bacteria emitted light for imaging and hydrolyzed the glucuronide prodrug 9ACG to the topoisomerase I inhibitor 9-aminocamptothecin (9AC). By optical imaging, colony-forming units (CFUs) and staining for bG activity, we found that DH5a-lux/bG preferentially localized and replicated within CL1-5 human lung tumors in mice. The intensity of luminescence, CFU and bG activity increased with time, indicating bacterial replication occurred in tumors. In comparison with DH5a-lux/bG, 9AC or 9ACG treatment, combined systemic administration of DH5a-lux/bG followed by 9ACG prodrug treatment significantly (Po0.005) delayed the growth of CL1-5 tumors. Our results demonstrate that prodrug-activating bacteria may be useful for selective cancer chemotherapy.

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Liver cancer is the second leading cause of cancer deaths in Taiwan as per the 2011 statistics and ranks fourth in cancer-related mortality in the world. Recent researches have shown that Antrodia cinnamomea, a Taiwan-specific medicinal mushroom, has biological activities, including hepatoprotection, anti-inflammation, antihepatitis B virus activity, and anticancer activity. In the present study, the antiproliferative activity and molecular mechanisms of antcin K, the most abundant ergostane triterpenoid from the fruiting bodies of basswood cultivated A. cinnamomea, were investigated using human hepatoma Hep 3B cells. The results showed that antcin K effectively reduced Hep 3B cells viability within 48 hours. Antcin K induced phosphatidylserine exposure, chromatin condensation, and DNA damage, but did not significantly increase autophagosome content or cause cell expansion and cell lysis. Thus, the principal mode of Hep 3B cells death induced by antcin K was apoptosis, rather than autophagy or necrosis. In-depth investigation of the molecular mechanisms revealed that antcin K first promoted reactive oxygen species generation and adenosine triphosphate depletion, leading to endoplasmic reticulum stress and resulting in mitochondrial membrane permeability changes. After losing the mitochondrial membrane potential, caspase-independent and caspase-dependent apoptosis-related proteins were released, including HtrA2, apoptotic-induced factor, endonuclease G, and cytochrome c. Cytochrome c activated caspase-9 and caspase-3, and cut downstream protein PARP, ultimately leading to cell apoptosis. These results suggested that antcin K induced mitochondrial and endoplasmic reticulum stress-mediated apoptosis in human hepatoma cells. Coupled with these findings, antcin K has a potential to be a complementary agent in liver cancer therapy.