Progressive Transient Photon Beams

In this work we introduce a novel algorithm for transient rendering in participating media. Our method is consistent, robust, and is able to generate animations of time-resolved light transport featuring complex caustic light paths in media. We base our method on the observation that the spatial continuity provides an increased coverage of the temporal domain, and generalize photon beams to transient-state. We extend the beam steady-state radiance estimates to include the temporal domain. Then, we develop a progressive version of spatio-temporal density estimations, that converges to the correct solution with finite memory requirements by iteratively averaging several realizations of independent renders with a progressively reduced kernel bandwidth. We derive the optimal convergence rates accounting for space and time kernels, and demonstrate our method against previous consistent transient rendering methods for participating media

Sub-Doppler spectroscopy of Rb atoms in a sub-micron vapor cell in the presence of a magnetic field

We report the first use of an extremely thin vapor cell (thickness ~ 400 nm) to study the magnetic-field dependence of laser-induced-fluorescence excitation spectra of alkali atoms. This thin cell allows for sub-Doppler resolution without the complexity of atomic beam or laser cooling techniques. This technique is used to study the laser-induced-fluorescence excitation spectra of Rb in a 50 G magnetic field. At this field strength the electronic angular momentum J and nuclear angular momentum I are only partially decoupled. As a result of the mixing of wavefunctions of different hyperfine states, we observe a nonlinear Zeeman effect for each sublevel, a substantial modification of the transition probabilities between different magnetic sublevels, and the appearance of transitions that are strictly forbidden in the absence of the magnetic field. For the case of right- and left- handed circularly polarized laser excitation, the fluorescence spectra differs qualitatively. Well pronounced magnetic field induced circular dichroism is observed. These observations are explained with a standard approach that describes the partial decoupling of I and J states

Adjoint "quarks" on coarse anisotropic lattices: Implications for string breaking in full QCD

A detailed study is made of four dimensional SU(2) gauge theory with static adjoint ``quarks'' in the context of string breaking. A tadpole-improved action is used to do simulations on lattices with coarse spatial spacings $a_s$, allowing the static potential to be probed at large separations at a dramatically reduced computational cost. Highly anisotropic lattices are used, with fine temporal spacings $a_t$, in order to assess the behavior of the time-dependent effective potentials. The lattice spacings are determined from the potentials for quarks in the fundamental representation. Simulations of the Wilson loop in the adjoint representation are done, and the energies of magnetic and electric ``gluelumps'' (adjoint quark-gluon bound states) are calculated, which set the energy scale for string breaking. Correlators of gauge-fixed static quark propagators, without a connecting string of spatial links, are analyzed. Correlation functions of gluelump pairs are also considered; similar correlators have recently been proposed for observing string breaking in full QCD and other models. A thorough discussion of the relevance of Wilson loops over other operators for studies of string breaking is presented, using the simulation results presented here to support a number of new arguments.Comment: 22 pages, 14 figure

Balancing repair and tolerance of DNA damage caused by alkylating agents

Alkylating agents constitute a major class of frontline chemotherapeutic drugs that inflict cytotoxic DNA damage as their main mode of action, in addition to collateral mutagenic damage. Numerous cellular pathways, including direct DNA damage reversal, base excision repair (BER) and mismatch repair (MMR), respond to alkylation damage to defend against alkylation-induced cell death or mutation. However, maintaining a proper balance of activity both within and between these pathways is crucial for a favourable response of an organism to alkylating agents. Furthermore, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylating agent toxicity

The Cycad Genotoxin MAM Modulates Brain Cellular Pathways Involved in Neurodegenerative Disease and Cancer in a DNA Damage-Linked Manner

Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of adult C57BL6 wild-type mice treated with a single systemic dose of MAM acetate display DNA damage (O6-methyldeoxyguanosine lesions, O6-mG) that remains constant up to 7 days post-treatment. By contrast, MAM-treated mice lacking a functional gene encoding the DNA repair enzyme O6-mG DNA methyltransferase (MGMT) showed elevated O6-mG DNA damage starting at 48 hours post-treatment. The DNA damage was linked to changes in the expression of genes in cell-signaling pathways associated with cancer, human neurodegenerative disease, and neurodevelopmental disorders. These data are consistent with the established developmental neurotoxic and carcinogenic properties of MAM in rodents. They also support the hypothesis that early-life exposure to MAM-glucoside (cycasin) has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for food or medicine, or both. These findings suggest environmental genotoxins, specifically MAM, target common pathways involved in neurodegeneration and cancer, the outcome depending on whether the cell can divide (cancer) or not (neurodegeneration). Exposure to MAM-related environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimer's disease