Investigation of Quantum Phase Transitions using Multi-target DMRG Methods

In this paper we examine how the predictions of conformal invariance can be widely exploited to overcome the difficulties of the density-matrix renormalization group near quantum critical points. The main idea is to match the set of low-lying energy levels of the lattice Hamiltonian, as a function of the system's size, with the spectrum expected for a given conformal field theory in two dimensions. As in previous studies this procedure requires an accurate targeting of various excited states. Here we discuss how this can be achieved within the DMRG algorithm by means of the recently proposed Thick-restart Lanczos method. As a nontrivial benchmark we use an anisotropic spin-1 Hamiltonian with special attention to the transitions from the Haldane phase. Nonetheless, we think that this procedure could be generally valid in the study of quantum critical phenomena.Comment: 14 pages, LaTeX2e (svjour class), 8 EPS figures. Same version as the published one, with new references and English corrections of the proofreade

Septic rupture of the ascending aorta after aortocoronary bypass surgery

We describe an exceptional case of non-fatal septic rupture of the ascending aorta in a patient with sternal dehiscence, deep sternal wound infection (DSWI) and pleural empyema after aortocoronary bypass surgery. Routine follow-up computed tomography (CT) detected a mediastinal pseudoaneurysm originating from the ascending aorta. Thereby, massive and irregular sternal bone defects and contrast-enhancing mediastinal soft tissue suggest osteomyelitis and highly-active and aggressive DSWI as initial triggers. Urgent thoracotomy 1 day later included ascending aorta reconstruction, total sternum resection and broad wound debridement. Follow-up CT 1 year later showed a regular postoperative result in a fully recovered patient

On a clear day you can see forever : integrating values and skills in sex offender treatment

The topic of sex offender rehabilitation frequently evokes fierce reactions, ranging from strident demands for harsher sentences contrasted with calls for more imaginative and compassionate sentencing options. There seems to be a polarization of positions centred on the question of offenders\u27 moral standing: are they moral strangers or fellow travellers? This fundamental disagreement about offenders\u27 moral status is at the core of a number of independent, although related current practice and research issues confronting the field, namely: (1) risk management versus strength-based treatment approaches; (2) the utility of utilizing individually tailored versus manual-based programmes for offenders; (3) focusing on the technical aspects or therapy as opposed to relationship and therapist factors (what has been called process issues); and (4) the conflict between protecting the community versus promoting the interests of offenders. In this paper I suggest that an approach to sex offender treatment based on a combination of human rights theory (an ethical resource) and strengths-based approaches can help us navigate our way through the above dilemmas in a way that addressees both the needs of offenders and those of the community

Ground state and stability of the fractional plateau phase in metallic Shastry Sutherland system TmB4

We present a study of the ground state and stability of the fractional plateau phase FPP with M Msat 1 8 in the metallic Shastry Sutherland system TmB4. Magnetization M measurements show that the FPP states are thermodynamically stable when the sample is cooled in constant magnetic field from the paramagnetic phase to the ordered one at 2 K. On the other hand, after zero field cooling and subsequent magnetization these states appear to be of dynamic origin. In this case the FPP states are closely associated with the half plateau phase HPP, M Msat , mediate the HPP to the low field antiferromagnetic AF phase and depend on the thermodynamic history. Thus, in the same place of the phase diagram both, the stable and the metastable dynamic fractional plateau FP states, can be observed, depending on the way they are reached. In case of metastable FP states thermodynamic paths are identified that lead to very flat fractional plateaus in the FPP. Moreover, with a further decrease of magnetic field also the low field AF phase becomes influenced and exhibits a plateau of the order of 1 1000 Msa

Systems-Level Modeling of Cancer-Fibroblast Interaction

Cancer cells interact with surrounding stromal fibroblasts during tumorigenesis, but the complex molecular rules that govern these interactions remain poorly understood thus hindering the development of therapeutic strategies to target cancer stroma. We have taken a mathematical approach to begin defining these rules by performing the first large-scale quantitative analysis of fibroblast effects on cancer cell proliferation across more than four hundred heterotypic cell line pairings. Systems-level modeling of this complex dataset using singular value decomposition revealed that normal tissue fibroblasts variably express at least two functionally distinct activities, one which reflects transcriptional programs associated with activated mesenchymal cells, that act either coordinately or at cross-purposes to modulate cancer cell proliferation. These findings suggest that quantitative approaches may prove useful for identifying organizational principles that govern complex heterotypic cell-cell interactions in cancer and other contexts

The role of tenascin-C in tissue injury and tumorigenesis

The extracellular matrix molecule tenascin-C is highly expressed during embryonic development, tissue repair and in pathological situations such as chronic inflammation and cancer. Tenascin-C interacts with several other extracellular matrix molecules and cell-surface receptors, thus affecting tissue architecture, tissue resilience and cell responses. Tenascin-C modulates cell migration, proliferation and cellular signaling through induction of pro-inflammatory cytokines and oncogenic signaling molecules amongst other mechanisms. Given the causal role of inflammation in cancer progression, common mechanisms might be controlled by tenascin-C during both events. Drugs targeting the expression or function of tenascin-C or the tenascin-C protein itself are currently being developed and some drugs have already reached advanced clinical trials. This generates hope that increased knowledge about tenascin-C will further improve management of diseases with high tenascin-C expression such as chronic inflammation, heart failure, artheriosclerosis and cancer

The activation of Proteinase-Activated Receptor-1 (PAR1) mediates gastric cancer cell proliferation and invasion

<p>Abstract</p> <p>Background</p> <p>In addition to regulating platelet function, the G protein-coupled sub-family member Proteinase-activated receptor-1 (PAR1) has a proposed role in the development of various cancers, but its exact role and mechanism of action in the invasion, metastasis, and proliferation process in gastric cancer have yet to be completely elucidated. Here, we analyzed the relationship between PAR1 activation, proliferation, invasion, and the signaling pathways downstream of PAR1 activation in gastric cancer.</p> <p>Methods</p> <p>We established a PAR1 stably transfected MKN45 human gastric cancer cell line (MKN45/PAR1) and performed cell proliferation and invasion assays employing this cell line and MKN28 cell line exposed to PAR1 agonists (α-thrombin and TFLLR-NH₂). We also quantified NF-κB activation by electrophoretic mobility shift assay (EMSA) and the level of Tenascin-C (TN-C) expression in conditioned medium by ELISA of MKN45/PAR1 following administration of α-thrombin. A high molecular weight concentrate was derived from the resultant conditioned medium and subsequent cultures of MKN45/PAR1 and MKN28 were exposed to the resultant concentrate either in the presence or absence of TN-C-neutralizing antibody. Lysates of these subsequent cells were probed to quantify levels of phospholyrated Epidermal Growth Factor Receptor (EGFR).</p> <p>Result</p> <p>PAR1 in both PAR1/MKN45 and MKN28 was activated by PAR1 agonists, resulting in cell proliferation and matrigel invasion. We have shown that activation of NF-κB and EGFR phosphorylation initially were triggered by the activation of PAR1 with α-thrombin. Quantitative PCR and Western blot assay revealed up-regulation of mRNA and protein expression of NF-κB target genes, especially TN-C, a potential EGFR activator. The suppressed level of phosphorylated EGFR, observed in cells exposed to concentrate of conditioned medium in the presence of TN-C-neutralizing antibody, identifies TN-C as a putative autocrine stimulatory factor of EGFR possibly involved in the sustained PAR1 activation responses observed.</p> <p>Conclusion</p> <p>Our data indicate that in gastric carcinoma cells, PAR1 activation can trigger an array of responses that would promote tumor cell growth and invasion. Over expression of NF-κB, EGFR, and TN-C, are among the effects of PAR1 activation and TN-C induces EGFR activation in an autocrine manner. Thus, PAR1 is a potentially important therapeutic target for the treatment of gastric cancer.</p

Advances in tenascin-C biology

Tenascin-C is an extracellular matrix glycoprotein that is specifically and transiently expressed upon tissue injury. Upon tissue damage, tenascin-C plays a multitude of different roles that mediate both inflammatory and fibrotic processes to enable effective tissue repair. In the last decade, emerging evidence has demonstrated a vital role for tenascin-C in cardiac and arterial injury, tumor angiogenesis and metastasis, as well as in modulating stem cell behavior. Here we highlight the molecular mechanisms by which tenascin-C mediates these effects and discuss the implications of mis-regulated tenascin-C expression in driving disease pathology