424 research outputs found
Analysis of two-player quantum games in an EPR setting using geometric algebra
The framework for playing quantum games in an Einstein-Podolsky-Rosen (EPR)
type setting is investigated using the mathematical formalism of Clifford
geometric algebra (GA). In this setting, the players' strategy sets remain
identical to the ones in the classical mixed-strategy version of the game,
which is then obtained as proper subset of the corresponding quantum game. As
examples, using GA we analyze the games of Prisoners' Dilemma and Stag Hunt
when played in the EPR type setting.Comment: 20 pages, no figure, revise
Targeting prostate cancer based on signal transduction and cell cycle pathways
Prostate cancer remains a leading cause of death in men despite increased capacity to diagnose at earlier stages. After prostate cancer has become hormone independent, which often occurs after hormonal ablation therapies, it is difficult to effectively treat. Prostate cancer may arise from mutations and dysregulation of various genes involved in regulation signal transduction (e.g., PTEN, Akt, etc.,) and the cell cycle (e.g., p53, p21Cip1, p27Kip1, Rb, etc.,). This review focuses on the aberrant interactions of signal transduction and cell cycle genes products and how they can contribute to prostate cancer and alter therapeutic effectiveness. Originally published Cell Cycle, Vol. 7, No. 12, June 200
N-player quantum games in an EPR setting
The -player quantum game is analyzed in the context of an
Einstein-Podolsky-Rosen (EPR) experiment. In this setting, a player's
strategies are not unitary transformations as in alternate quantum
game-theoretic frameworks, but a classical choice between two directions along
which spin or polarization measurements are made. The players' strategies thus
remain identical to their strategies in the mixed-strategy version of the
classical game. In the EPR setting the quantum game reduces itself to the
corresponding classical game when the shared quantum state reaches zero
entanglement. We find the relations for the probability distribution for
-qubit GHZ and W-type states, subject to general measurement directions,
from which the expressions for the mixed Nash equilibrium and the payoffs are
determined. Players' payoffs are then defined with linear functions so that
common two-player games can be easily extended to the -player case and
permit analytic expressions for the Nash equilibrium. As a specific example, we
solve the Prisoners' Dilemma game for general . We find a new
property for the game that for an even number of players the payoffs at the
Nash equilibrium are equal, whereas for an odd number of players the
cooperating players receive higher payoffs.Comment: 26 pages, 2 figure
Revisiting special relativity: A natural algebraic alternative to Minkowski spacetime
Minkowski famously introduced the concept of a space-time continuum in 1908,
merging the three dimensions of space with an imaginary time dimension , with the unit imaginary producing the correct spacetime distance , and the results of Einstein's then recently developed theory of special
relativity, thus providing an explanation for Einstein's theory in terms of the
structure of space and time. As an alternative to a planar Minkowski space-time
of two space dimensions and one time dimension, we replace the unit imaginary , with the Clifford bivector for the plane
that also squares to minus one, but which can be included without the addition
of an extra dimension, as it is an integral part of the real Cartesian plane
with the orthonormal basis and . We find that with this model of
planar spacetime, using a two-dimensional Clifford multivector, the spacetime
metric and the Lorentz transformations follow immediately as properties of the
algebra. This also leads to momentum and energy being represented as components
of a multivector and we give a new efficient derivation of Compton's scattering
formula, and a simple formulation of Dirac's and Maxwell's equations. Based on
the mathematical structure of the multivector, we produce a semi-classical
model of massive particles, which can then be viewed as the origin of the
Minkowski spacetime structure and thus a deeper explanation for relativistic
effects. We also find a new perspective on the nature of time, which is now
given a precise mathematical definition as the bivector of the plane.Comment: 29 pages, 2 figure
Recommended from our members
Best practices to maximize the use and reuse of quantitative and systems pharmacology models: recommendations from the United Kingdom quantitative and systems pharmacology network
The lack of standardization in the way that quantitative and systems pharmacology (QSP) models are developed, tested, and documented hinders their reproducibility, reusability, and expansion or reduction to alternative contexts. This in turn undermines the potential impact of QSP in academic, industrial, and regulatory frameworks. This article presents a minimum set of recommendations from the UK Quantitative and Systems Pharmacology Network (UK QSP Network) to guide QSP practitioners seeking to maximize their impact, and stakeholders considering the use of QSP models in their environment
Roles of the RAF/MEK/ERK Pathway in Cell Growth, Malignant Transformation and Drug Resistance
Growth factors and mitogens use the Ras/Raf/MEK/ERK signaling cascade to transmit signals from their receptors to regulate gene expression and prevent apoptosis. Some components of these pathways are mutated or aberrantly expressed in human cancer (e.g., Ras, B-Raf). Mutations also occur at genes encoding upstream receptors (e.g., EGFR and Flt-3) and chimeric chromosomal translocations (e.g., BCR-ABL) which transmit their signals through these cascades. Even in the absence of obvious genetic mutations, this pathway has been reported to be activated in over 50% of acute myelogenous leukemia and acute lymphocytic leukemia and is also frequently activated in other cancer types (e.g., breast and prostate cancers). Importantly, this increased expression is associated with a poor prognosis. The Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt pathways interact with each other to regulate growth and in some cases tumorigenesis. For example, in some cells, PTEN mutation may contribute to suppression of the Raf/MEK/ERK cascade due to the ability of activated Akt to phosphorylate and inactivate different Rafs. Although both of these pathways are commonly thought to have anti-apoptotic and drug resistance effects on cells, they display different cell lineage specific effects. For example, Raf/MEK/ERK is usually associated with proliferation and drug resistance of hematopoietic cells, while activation of the Raf/MEK/ERK cascade is suppressed in some prostate cancer cell lines which have mutations at PTEN and express high levels of activated Akt. Furthermore the Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt pathways also interact with the p53 pathway. Some of these interactions can result in controlling the activity and subcellular localization of Bim, Bak, Bax, Puma and Noxa. Raf/MEK/ERK may promote cell cycle arrest in prostate cells and this may be regulated by p53 as restoration of wild-type p53 in p53 deficient prostate cancer cells results in their enhanced sensitivity to chemotherapeutic drugs and increased expression of Raf/MEK/ERK pathway. Thus in advanced prostate cancer, it may be advantageous to induce Raf/MEK/ERK expression to promote cell cycle arrest, while in hematopoietic cancers it may be beneficial to inhibit Raf/MEK/ERK induced proliferation and drug resistance. Thus the Raf/MEK/ERK pathway has different effects on growth, prevention of apoptosis, cell cycle arrest and induction of drug resistance in cells of various lineages which may be due to the presence of functional p53 and PTEN and the expression of lineage specific factors. Originally published Biochim Biophys Acta, Vol. 1773, No. 8, August 200
Middle East respiratory syndrome
The Middle East respiratory syndrome is caused by a coronavirus that was first identified in Saudi Arabia in 2012. Periodic outbreaks continue to occur in the Middle East and elsewhere. This report provides the latest information on MERS
Cellular senescence impairs the reversibility of pulmonary arterial hypertension
Pulmonary arterial hypertension (PAH) in congenital cardiac shunts can be reversed by hemodynamic unloading (HU) through shunt closure. However, this reversibility potential is lost beyond a certain point in time. The reason why PAH becomes irreversible is unknown. In this study, we used MCT+shunt-induced PAH in rats to identify a dichotomous reversibility response to HU, similar to the human situation. We compared vascular profiles of reversible and irreversible PAH using RNA sequencing. Cumulatively, we report that loss of reversibility is associated with a switch from a proliferative to a senescent vascular phenotype and confirmed markers of senescence in human PAH-CHD tissue. In vitro, we showed that human pulmonary endothelial cells of patients with PAH are more vulnerable to senescence than controls in response to shear stress and confirmed that the senolytic ABT263 induces apoptosis in senescent, but not in normal, endothelial cells. To support the concept that vascular cell senescence is causal to the irreversible nature of end-stage PAH, we targeted senescence using ABT263 and induced reversal of the hemodynamic and structural changes associated with severe PAH refractory to HU. The factors that drive the transition from a reversible to irreversible pulmonary vascular phenotype could also explain the irreversible nature of other PAH etiologies and provide new leads for pharmacological reversal of end-stage PAH
- …