Budd-Chiari syndrome recurring in a transplanted liver

A patient with Budd-Chiari syndrome who underwent orthotopic liver transplantation and developed recurrent disease is described. The immediate postoperative period was complicated by multiple thrombotic episodes, followed by a period of apparent remission associated with the initiation of coumadin and persantine therapy. After discontinuation of such antithrombotic therapy in order to biopsy the liver, the patient experienced another series of clinically overt vascular thromboses and ultimately died of sepsis 15 mo posttransplantation after a prolonged and complicated terminal hospital course. At autopsy, recurrent Budd-Chiari syndrome as well as thromboses in numerous other organs was demonstrated. © 1983

The Clumping Transition in Niche Competition: a Robust Critical Phenomenon

We show analytically and numerically that the appearance of lumps and gaps in the distribution of n competing species along a niche axis is a robust phenomenon whenever the finiteness of the niche space is taken into account. In this case depending if the niche width of the species $\sigma$ is above or below a threshold $\sigma_c$, which for large n coincides with 2/n, there are two different regimes. For $\sigma > sigma_c$ the lumpy pattern emerges directly from the dominant eigenvector of the competition matrix because its corresponding eigenvalue becomes negative. For $\sigma </- sigma_c$ the lumpy pattern disappears. Furthermore, this clumping transition exhibits critical slowing down as $\sigma$ is approached from above. We also find that the number of lumps of species vs. $\sigma$ displays a stair-step structure. The positions of these steps are distributed according to a power-law. It is thus straightforward to predict the number of groups that can be packed along a niche axis and it coincides with field measurements for a wide range of the model parameters.Comment: 16 pages, 7 figures; http://iopscience.iop.org/1742-5468/2010/05/P0500

A model for the induction of chromosome aberrations through direct and bystander mechanisms

A state vector model (SVM) for chromosome aberrations and neoplastic transformation has been adapted to describe detrimental bystander effects. The model describes initiation (formation of translocations) and promotion (clonal expansion and loss of contact inhibition of initiated cells). Additional terms either in the initiation model or in the rate of clonal expansion of initiated cells, describe detrimental bystander effects for chromosome aberrations as reported in the scientific literature. In the present study, the SVM with bystander effects is tested on a suitable dataset. In addition to the simulation of non-linear effects, a classical dataset for neoplastic transformation in C3H 10T1/2 cells after alpha particle irradiation is used to show that the model without bystander features can also describe LNT-like dose responses. A published model for bystander induced neoplastic transformation was adapted for chromosome aberration induction and used to compare the results obtained with the different models

Systems biological and mechanistic modelling of radiation-induced cancer

This paper summarises the five presentations at the First International Workshop on Systems Radiation Biology that were concerned with mechanistic models for carcinogenesis. The mathematical description of various hypotheses about the carcinogenic process, and its comparison with available data is an example of systems biology. It promises better understanding of effects at the whole body level based on properties of cells and signalling mechanisms between them. Of these five presentations, three dealt with multistage carcinogenesis within the framework of stochastic multistage clonal expansion models, another presented a deterministic multistage model incorporating chromosomal aberrations and neoplastic transformation, and the last presented a model of DNA double-strand break repair pathways for second breast cancers following radiation therapy

Detrimental and Protective Bystander Effects: A Model Approach

This work integrates two important cellular responses to low doses, detrimental bystander effects and apoptosis-mediated protective bystander effects, into a multistage model for chromosome aberrations and in vitro neoplastic transformation: the State-Vector Model. The new models were tested on representative data sets that show supralinear or U-shaped dose responses. The original model without the new low-dose features was also tested for consistency with LNT-shaped dose responses. Reductions of in vitro neoplastic transformation frequencies below the spontaneous level have been reported after exposure of cells to low doses of low-LET radiation. In the current study, this protective effect is explained with by-stander-induced apoptosis. An important data set that shows a low-dose detrimental bystander effect for chromosome aberrations was successfully fitted by additional terms within the cell initiation stage. It was found that this approach is equivalent to bystander-induced clonal expansion of initiated cells. This study is an important step toward a comprehensive model that contains all essential biological mechanisms that can influence dose–response curves at low doses

Gauge invariance and finite width effects in radiative two-pion tau lepton decay

The contribution of the rho^{\pm} vector meson to the tau -> pi pi nu gamma decay is considered as a potential source for the determination of the magnetic dipole moment of this light vector meson. In order to keep gauge-invariance of the whole decay amplitude, a procedure similar to the fermion loop-scheme for charged gauge bosons is implemented to incorporate the finite width effects of the rho^{\pm} vector meson. The absorptive pieces of the one-loop corrections to the propagators and electromagnetic vertices of the rho^{\pm} meson and W^{\pm} gauge boson have identical forms in the limit of massless particles in the loops, suggesting this to be a universal feature of spin-one unstable particles. Model-dependent contributions to the tau -> pi pi nu gamma decay are suppressed by fixing the two-pion invariant mass distribution at the rho meson mass value. The resulting photon energy and angular distribution is relatively sensitive to the effects of the rho magnetic dipole moment.Comment: 22 pages, 4 postscript figures, references and comments on relevance of perturbative treatment of rho electromagnetic vertex are added, accepted for pub. in Phys. Rev.

A new Perspective on the Scalar meson Puzzle, from Spontaneous Chiral Symmetry Breaking Beyond BCS

We introduce coupled channels of Bethe-Salpeter mesons both in the boundstate equation for mesons and in the mass gap equation for chiral symmetry. Consistency is insured by the Ward Identities for axial currents, which preserve the Goldstone boson nature of the pion and prevents a systematic shift of the hadron spectrum. We study the decay of a scalar meson coupled to a pair of pseudoscalars. We also show that coupled channels reduce the breaking of chiral symmetry, with the same Feynman diagrams that appear in the coupling of a scalar meson to a pair of pseudoscalar mesons. Exact calculations are performed in a particular confining quark model, where we find that the groundstate $I=0, ^3P_0 q \bar q$ meson is the f_0(980) with a partial decay width of 40MeV. We also find a 30% reduction of the chiral condensate due to coupled channels.Comment: 17 pages, Revtex, 8 eps figures, and several eps diagrams in equation

Thoracolumbar injury classification and severity score: a new paradigm for the treatment of thoracolumbar spine trauma

BACKGROUND: Contemporary understanding of the biomechanics, natural history, and methods of treating thoracolumbar spine injuries continues to evolve. Current classification schemes of these injuries, however, can be either too simplified or overly complex for clinical use. METHODS: The Spine Trauma Group was given a survey to identify similarities in treatment algorithms for common thoracolumbar injuries, as well as to identify characteristics of injury that played a key role in the decision-making process. RESULTS: Based on the survey, the Spine Trauma Group has developed a classification system and an injury severity score (thoracolumbar injury classification and severity score, or TLICS), which may facilitate communication between physicians and serve as a guideline for treating these injuries. The classification system is based on the morphology of the injury, integrity of the posterior ligamentous complex, and neurological status of the patient. Points are assigned for each category, and the final total points suggest a possible treatment option. CONCLUSIONS: The usefulness of this new system will have to be proven in future studies investigating inter- and intraobserver reliability, as well as long-term outcome studies for operative and nonoperative treatment methods