Geodesic distances on density matrices

We find an upper bound for geodesic distances associated to monotone Riemannian metrics on positive definite matrices and density matrices.Comment: 10 page

A new experimental tool to overcome a misconception concerning heat and internal energy

Nous présentons un dispositif expérimental permettant de faire comprendre aux étudiants la différence existant entre chaleur et énergie interne.An experimental device is presented to overcome the difficulties encountered by students when studying heat and internal energy

Radiotherapy planning for glioblastoma based on a tumor growth model: Improving target volume delineation

Glioblastoma are known to infiltrate the brain parenchyma instead of forming a solid tumor mass with a defined boundary. Only the part of the tumor with high tumor cell density can be localized through imaging directly. In contrast, brain tissue infiltrated by tumor cells at low density appears normal on current imaging modalities. In clinical practice, a uniform margin is applied to account for microscopic spread of disease. The current treatment planning procedure can potentially be improved by accounting for the anisotropy of tumor growth: Anatomical barriers such as the falx cerebri represent boundaries for migrating tumor cells. In addition, tumor cells primarily spread in white matter and infiltrate gray matter at lower rate. We investigate the use of a phenomenological tumor growth model for treatment planning. The model is based on the Fisher-Kolmogorov equation, which formalizes these growth characteristics and estimates the spatial distribution of tumor cells in normal appearing regions of the brain. The target volume for radiotherapy planning can be defined as an isoline of the simulated tumor cell density. A retrospective study involving 10 glioblastoma patients has been performed. To illustrate the main findings of the study, a detailed case study is presented for a glioblastoma located close to the falx. In this situation, the falx represents a boundary for migrating tumor cells, whereas the corpus callosum provides a route for the tumor to spread to the contralateral hemisphere. We further discuss the sensitivity of the model with respect to the input parameters. Correct segmentation of the brain appears to be the most crucial model input. We conclude that the tumor growth model provides a method to account for anisotropic growth patterns of glioblastoma, and may therefore provide a tool to make target delineation more objective and automated

Radiation-induced caveolin-1 associated EGFR internalization is linked with nuclear EGFR transport and activation of DNA-PK

<p>Abstract</p> <p>Background</p> <p>To elucidate the role of src kinase in caveolin-1 driven internalization and nuclear transport of EGFR linked to regulation of DNA-repair in irradiated cells.</p> <p>Results</p> <p>Ionizing radiation resulted in src kinase stabilization, activation and subsequent src mediated caveolin-1 Y14- and EGFR Y845-phosphorylations. Both phosphorylations were radiation specific and could not be observed after treatment with EGF. Inhibition of EGFR by the antibody Erbitux resulted in a strong accumulation of caveolin/EGFR complexes within the cytoplasm, which could not be further increased by irradiation. Radiation-induced caveolin-1- and EGFR-phosphorylations were associated with nuclear EGFR transport and activation of DNA-PK, as detected by phosphorylation at T2609. Blockage of src activity by the specific inhibitor PP2, decreased nuclear transport of EGFR and inhibited caveolin-1- and DNA-PK-phosphorylation. Knockdown of src by specific siRNA blocked EGFR phosphorylation at Y845, phosphorylation of caveolin-1 at Y14 and abolished EGFR transport into the nucleus and phosphorylation of DNA-PK. Consequently, both knockdown of src by specific siRNA and also inhibition of src activity by PP2 resulted in an enhanced residual DNA-damage as quantified 24 h after irradiation and increased radiosensitivity.</p> <p>Conclusion</p> <p>Src kinase activation following irradiation triggered caveolin-1 dependent EGFR internalization into caveolae. Subsequently EGFR shuttled into the nucleus. As a consequence, inhibition of internalization and nuclear transport of EGFR blocked radiation-induced phosphorylation of DNA-PK and hampered repair of radiation-induced double strand breaks.</p

Two-Qubit Separability Probabilities and Beta Functions

Due to recent important work of Zyczkowski and Sommers (quant-ph/0302197 and quant-ph/0304041), exact formulas are available (both in terms of the Hilbert-Schmidt and Bures metrics) for the (n^2-1)-dimensional and (n(n-1)/2-1)-dimensional volumes of the complex and real n x n density matrices. However, no comparable formulas are available for the volumes (and, hence, probabilities) of various separable subsets of them. We seek to clarify this situation for the Hilbert-Schmidt metric for the simplest possible case of n=4, that is, the two-qubit systems. Making use of the density matrix (rho) parameterization of Bloore (J. Phys. A 9, 2059 [1976]), we are able to reduce each of the real and complex volume problems to the calculation of a one-dimensional integral, the single relevant variable being a certain ratio of diagonal entries, nu = (rho_{11} rho_{44})/{rho_{22} rho_{33})$. The associated integrand in each case is the product of a known (highly oscillatory near nu=1) jacobian and a certain unknown univariate function, which our extensive numerical (quasi-Monte Carlo) computations indicate is very closely proportional to an (incomplete) beta function B_{nu}(a,b), with a=1/2, b=sqrt{3}in the real case, and a=2 sqrt{6}/5, b =3/sqrt{2} in the complex case. Assuming the full applicability of these specific incomplete beta functions, we undertake separable volume calculations.Comment: 17 pages, 4 figures, paper is substantially rewritten and reorganized, with the quasi-Monte Carlo integration sample size being greatly increase

Antigens in human glioblastomas and meningiomas: Search for tumour and onco-foetal antigens. Estimation of S-100 and GFA protein.

Extracts of glioblastomas and meningiomas were analysed by quantitative immunoelectrophoresis for the presence of foetal brain antigens and tumour-associated antigens, and levels of 2 normal brain-specific proteins were also determined. The following antibodies were used: monospecific anti-S-100 (glia specific); monospecific anti-GFA (glial fibrillary acidic protein), (astroglia specific); polyspecific anti-foetal brain (12-16th week of gestation); a polyspecific anti-glioblastoma antiserum, absorbed with insolubilized serum, haemolysate and normal brain extract; polyspecific anti-alpha-foetoprotein; and monospecific anti-ferritin. Using the antibodies raised against the tumours, several antigens not present in foetal or adult normal brain were found in the glioblastomas and the meningiomas. These antigens cross-reacted with antigens present in normal liver and were therefore not tumour-associated. S-100 was found in glioblastomas in approximately one tenth the amount in whole brain homogenate, whereas GFA was found 2-4 times enriched. The 2 proteins were absent in meningiomas. The possible use of the GFA protein as a marker for astroglial neoplasia is discussed. Five foetal antigens were found in foetal brain, but none in the tumours. alpha-Foetoprotein could only be demonstrated in foetal tissue extracts, including foetal brain, but not in tumours. Ferritin was detected in all tumour extracts, although the amounts determined were unrelated to histological tumour type

Effective lattice theories for Polyakov loops

We derive effective actions for SU(2) Polyakov loops using inverse Monte Carlo techniques. In a first approach, we determine the effective couplings by requiring that the effective ensemble reproduces the single-site distribution of the Polyakov loops. The latter is flat below the critical temperature implying that the (untraced) Polyakov loop is distributed uniformly over its target space, the SU(2) group manifold. This allows for an analytic determination of the Binder cumulant and the distribution of the mean-field, which turns out to be approximately Gaussian. In a second approach, we employ novel lattice Schwinger-Dyson equations which reflect the SU(2) x SU(2) invariance of the functional Haar measure. Expanding the effective action in terms of SU(2) group characters makes the numerics sufficiently stable so that we are able to extract a total number of 14 couplings. The resulting action is short-ranged and reproduces the Yang-Mills correlators very well.Comment: 27 pages, 8 figures, v2: method refined, chapter and references adde

A Serpin shapes the extracellular environment to prevent influenza A virus maturation

Interferon-stimulated genes (ISGs) act in concert to provide a tight barrier against viruses. Recent studies have shed light on the contribution of individual ISG effectors to the antiviral state, but most have examined those acting on early, intracellular stages of the viral life cycle. Here, we applied an image-based screen to identify ISGs inhibiting late stages of influenza A virus (IAV) infection. We unraveled a directly antiviral function for the gene SERPINE1, encoding plasminogen activator inhibitor 1 (PAI-1). By targeting extracellular airway proteases, PAI-1 inhibits IAV glycoprotein cleavage, thereby reducing infectivity of progeny viruses. This was biologically relevant for IAV restriction in vivo. Further, partial PAI-1 deficiency, attributable to a polymorphism in human SERPINE1, conferred increased susceptibility to IAV in vitro. Together, our findings reveal that manipulating the extracellular environment to inhibit the last step in a virus life cycle is an important mechanism of the antiviral response

Bures volume of the set of mixed quantum states

We compute the volume of the N^2-1 dimensional set M_N of density matrices of size N with respect to the Bures measure and show that it is equal to that of a N^2-1 dimensional hyper-halfsphere of radius 1/2. For N=2 we obtain the volume of the Uhlmann 3-D hemisphere, embedded in R^4. We find also the area of the boundary of the set M_N and obtain analogous results for the smaller set of all real density matrices. An explicit formula for the Bures-Hall normalization constants is derived for an arbitrary N.Comment: 15 revtex pages, 2 figures in .eps; ver. 3, Eq. (4.19) correcte