Ferron-like states in YBa_2Cu_3O_(6+x)

With the use of the Hubbard model bound hole states in YBa_2Cu_3O_(6+x) are studied. For the parameters of this crystal the exchange interaction between the spin-carrying chain ion O^- and Cu-O plane sites is shown to ensure the formation of a large ferromagnetically ordered clusters around holes in the plane.Comment: 8 pages, 2 figure

<i>In Silico Oncology</i>: Quantification of the <i>In Vivo</i> Antitumor Efficacy of Cisplatin-Based Doublet Therapy in Non-Small Cell Lung Cancer (NSCLC) through a Multiscale Mechanistic Model

<div><p>The 5-year survival of non-small cell lung cancer patients can be as low as 1% in advanced stages. For patients with resectable disease, the successful choice of preoperative chemotherapy is critical to eliminate micrometastasis and improve operability. <i>In silico</i> experimentations can suggest the optimal treatment protocol for each patient based on their own multiscale data. A determinant for reliable predictions is the a priori estimation of the drugs’ cytotoxic efficacy on cancer cells for a given treatment. In the present work a mechanistic model of cancer response to treatment is applied for the estimation of a plausible value range of the cell killing efficacy of various cisplatin-based doublet regimens. Among others, the model incorporates the cancer related mechanism of uncontrolled proliferation, population heterogeneity, hypoxia and treatment resistance. The methodology is based on the provision of tumor volumetric data at two time points, before and after or during treatment. It takes into account the effect of tumor microenvironment and cell repopulation on treatment outcome. A thorough sensitivity analysis based on one-factor-at-a-time and latin hypercube sampling/partial rank correlation coefficient approaches has established the volume growth rate and the growth fraction at diagnosis as key features for more accurate estimates. The methodology is applied on the retrospective data of thirteen patients with non-small cell lung cancer who received cisplatin in combination with gemcitabine, vinorelbine or docetaxel in the neoadjuvant context. The selection of model input values has been guided by a comprehensive literature survey on cancer-specific proliferation kinetics. The latin hypercube sampling has been recruited to compensate for patient-specific uncertainties. Concluding, the present work provides a quantitative framework for the estimation of the <i>in-vivo</i> cell-killing ability of various chemotherapies. Correlation studies of such estimates with the molecular profile of patients could serve as a basis for reliable personalized predictions.</p></div

Main mechanism of action of cisplatin, gemcitabine, vinorelbine and docetaxel.

<p>Main mechanism of action of cisplatin, gemcitabine, vinorelbine and docetaxel.</p

Generic cell kinetic model for tumor response to chemotherapy.

<p>(A) Transition diagram between the five main cancer cell categories. (B) Cell cycle of cancer cells with proliferative capacity, either stem or LIMP (C) Cell cycle of cancer cells with proliferative capacity that are lethally hit by chemotherapy. Cells enter a rudimentary cell cycle that leads to apoptotic death from the phase dictated by the mechanism of action of the chemotherapeutic drug. In the schema, lethally hit cells are assumed to die at the end of S phase. Parameter symbols are explained in <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1005093#pcbi.1005093.t004" target="_blank">Table 4</a>. Abbreviations: LIMP: LImited Mitotic Potential tumor cell (also called committed or restricted progenitor cell), DIFF: terminally DIFFerentiated tumor cell, G1: Gap 1 cell cycle phase, S: DNA synthesis phase, G2: Gap 2 phase. M: Mitosis phase, G0: dormant, resting phase.</p

Baseline Values of Model Parameters Used in OFAT Sensitivity Analysis.

<p>Baseline Values of Model Parameters Used in OFAT Sensitivity Analysis.</p