57 research outputs found
Using Quasi-elastic Events to Measure Neutrino Oscillations with MINOS Detectors in the NuMI Neutrino Beam
MINOS (Main Injector Neutrino Oscillation Search) experiment has been designed
to search for a change in the
avor composition of a beam of muon neutrinos
as they travel between the Near Detector at Fermi National Accelerator Laboratory
and the Far Detector in the Soudan mine in Minnesota, 735 km from the target.
The MINOS oscillation analysis is mainly performed with the charged current
(CC) events and sensitive to constrain high-delta m2 values. However, the quasi-elastic
(QEL) charged current interaction is dominant in the energy region important to
access low-delta m2 values. For further improvement, the QEL oscillation analysis is performed
in this dissertation. A data sample based on a total of 2.50 x 1020 POT
is used for this analysis. In summary, 55 QEL-like events are observed at the
Far detector while 87.06 +/- 13.17 (syst:) events are expected with null oscillation
hypothesis. These data are consistent with vm disappearance via oscillation with
delta m2 = 2.10 +/- 0.37 (stat:) +/- 0.24 (syst:) eV2 and the maximal mixing angle
Reaction-diffusion kinetics on lattice at the microscopic scale
Lattice-based stochastic simulators are commonly used to study biological
reaction-diffusion processes. Some of these schemes that are based on the
reaction-diffusion master equation (RDME), can simulate for extended spatial
and temporal scales but cannot directly account for the microscopic effects in
the cell such as volume exclusion and diffusion-influenced reactions.
Nonetheless, schemes based on the high-resolution microscopic lattice method
(MLM) can directly simulate these effects by representing each finite-sized
molecule explicitly as a random walker on fine lattice voxels. The theory and
consistency of MLM in simulating diffusion-influenced reactions have not been
clarified in detail. Here, we examine MLM in solving diffusion-influenced
reactions in 3D space by employing the Spatiocyte simulation scheme. Applying
the random walk theory, we construct the general theoretical framework
underlying the method and obtain analytical expressions for the total rebinding
probability and the effective reaction rate. By matching Collins-Kimball and
lattice-based rate constants, we obtained the exact expressions to determine
the reaction acceptance probability and voxel size. We found that the size of
voxel should be about 2% larger than the molecule. MLM is validated by
numerical simulations, showing good agreement with the off-lattice
particle-based method, eGFRD. MLM run time is more than an order of magnitude
faster than eGFRD when diffusing macromolecules with typical concentrations in
the cell. MLM also showed good agreements with eGFRD and mean-field models in
case studies of two basic motifs of intracellular signaling, the protein
production-degradation process and the dual phosphorylation cycle. Moreover,
when a reaction compartment is populated with volume-excluding obstacles, MLM
captures the non-classical reaction kinetics caused by anomalous diffusion of
reacting molecules
Optical dispersions through intracellular inhomogeneities
Transport of intensity equation (TIE) exhibits a non-interferometric
correlation between intensity and phase variations of intermediate fields
(e.g., light and electron) in biological imaging. Previous TIE formulations
have generally assumed a free space propagation of monochromatic coherent field
functions crossing phase distributions along a longitudinal direction. Here, we
modify the TIE with fractal (or self-similar) organization models based on
intracellular refractive index turbulence. We then implement the TIE simulation
over a broad range of fractal dimensions and wavelengths. Simulation results
show how the intensity propagation through the spatial fluctuation of
intracellular refractive index interconnects fractal-dimensionality with
intensity dispersion (or transmissivity) within the picometer to micrometer
wavelength range. In addition, we provide a spatial-autocorrelation of phase
derivatives which allows the direct measurement and reconstruction of
intracellular fractal profiles from optical and electron microscopy imaging.Comment: 22 pages, 18 figures, 4 table
A computational framework for bioimaging simulation
Using bioimaging technology, biologists have attempted to identify and
document analytical interpretations that underlie biological phenomena in
biological cells. Theoretical biology aims at distilling those interpretations
into knowledge in the mathematical form of biochemical reaction networks and
understanding how higher level functions emerge from the combined action of
biomolecules. However, there still remain formidable challenges in bridging the
gap between bioimaging and mathematical modeling. Generally, measurements using
fluorescence microscopy systems are influenced by systematic effects that arise
from stochastic nature of biological cells, the imaging apparatus, and optical
physics. Such systematic effects are always present in all bioimaging systems
and hinder quantitative comparison between the cell model and bioimages.
Computational tools for such a comparison are still unavailable. Thus, in this
work, we present a computational framework for handling the parameters of the
cell models and the optical physics governing bioimaging systems. Simulation
using this framework can generate digital images of cell simulation results
after accounting for the systematic effects. We then demonstrate that such a
framework enables comparison at the level of photon-counting units.Comment: 57 page
Functional Interplay between P5 and PDI/ERp72 to Drive Protein Folding
The physiological functions of proteins are destined by their unique three-dimensional structures. Almost all biological kingdoms share conserved disulfide-catalysts and chaperone networks that assist in correct protein folding and prevent aggregation. Disruption of these networks is implicated in pathogenesis, including neurodegenerative disease. In the mammalian endoplasmic reticulum (ER), more than 20 members of the protein disulfide isomerase family (PDIs) are believed to cooperate in the client folding pathway, but it remains unclear whether complex formation among PDIs via non-covalent interaction is involved in regulating their enzymatic and chaperone functions. Herein, we report novel functional hetero complexes between PDIs that promote oxidative folding and inhibit aggregation along client folding. The findings provide insight into the physiological significance of disulfide-catalyst and chaperone networks and clues for understanding pathogenesis associated with disruption of the networks.P5 is one of protein disulfide isomerase family proteins (PDIs) involved in endoplasmic reticulum (ER) protein quality control that assists oxidative folding, inhibits protein aggregation, and regulates the unfolded protein response. P5 reportedly interacts with other PDIs via intermolecular disulfide bonds in cultured cells, but it remains unclear whether complex formation between P5 and other PDIs is involved in regulating enzymatic and chaperone functions. Herein, we established the far-western blot method to detect non-covalent interactions between P5 and other PDIs and found that PDI and ERp72 are partner proteins of P5. The enzymatic activity of P5-mediated oxidative folding is up-regulated by PDI, while the chaperone activity of P5 is stimulated by ERp72. These findings shed light on the mechanism by which the complex formations among PDIs drive to synergistically accelerate protein folding and prevents aggregation. This knowledge has implications for understanding misfolding-related pathology
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