Force Distribution in a Granular Medium

We report on systematic measurements of the distribution of normal forces exerted by granular material under uniaxial compression onto the interior surfaces of a confining vessel. Our experiments on three-dimensional, random packings of monodisperse glass beads show that this distribution is nearly uniform for forces below the mean force and decays exponentially for forces greater than the mean. The shape of the distribution and the value of the exponential decay constant are unaffected by changes in the system preparation history or in the boundary conditions. An empirical functional form for the distribution is proposed that provides an excellent fit over the whole force range measured and is also consistent with recent computer simulation data.Comment: 6 pages. For more information, see http://mrsec.uchicago.edu/granula

Power-Laws in Nonlinear Granular Chain under Gravity

The signal generated by a weak impulse propagates in an oscillatory way and dispersively in a gravitationally compacted granular chain. For the power-law type contact force, we show analytically that the type of dispersion follows power-laws in depth. The power-law for grain displacement signal is given by $h^{-1/4(1-1/p)}$ where $h$ and $p$ denote depth and the exponent of contact force, and the power-law for the grain velocity is $h^{-1/4({1/3}+1/p)}$. Other depth-dependent power-laws for oscillation frequency, wavelength, and period are given by combining above two and the phase velocity power-law $h^{1/2(1-1/p)}$. We verify above power-laws by comparing with the data obtained by numerical simulations.Comment: 12 pages, 3 figures; Changed conten

Kinetics and Jamming Coverage in a Random Sequential Adsorption of Polymer Chains

Using a highly efficient Monte Carlo algorithm, we are able to study the growth of coverage in a random sequential adsorption (RSA) of self-avoiding walk (SAW) chains for up to 10^{12} time steps on a square lattice. For the first time, the true jamming coverage (theta_J) is found to decay with the chain length (N) with a power-law theta_J propto N^{-0.1}. The growth of the coverage to its jamming limit can be described by a power-law, theta(t) approx theta_J -c/t^y with an effective exponent y which depends on the chain length, i.e., y = 0.50 for N=4 to y = 0.07 for N=30 with y -> 0 in the asymptotic limit N -> infinity.Comment: RevTeX, 5 pages inclduing figure

Capsid Antibodies to Different Adeno-Associated Virus Serotypes Bind Common Regions

Interactions between viruses and the host antibody immune response are critical in the development and control of disease, and antibodies are also known to interfere with the efficacy of viral vector-based gene delivery. The adeno-associated viruses (AAVs) being developed as vectors for corrective human gene delivery have shown promise in clinical trials, but preexisting antibodies are detrimental to successful outcomes. However, the antigenic epitopes on AAV capsids remain poorly characterized. Cryo-electron microscopy and three-dimensional image reconstruction were used to define the locations of epitopes to which monoclonal fragment antibodies (Fabs) against AAV1, AAV2, AAV5, and AAV6 bind. Pseudoatomic modeling showed that, in each serotype, Fabs bound to a limited number of sites near the protrusions surrounding the 3-fold axes of the T=1 icosahedral capsids. For the closely related AAV1 and AAV6, a common Fab exhibited substoichiometric binding, with one Fab bound, on average, between two of the three protrusions as a consequence of steric crowding. The other AAV Fabs saturated the capsid and bound to the walls of all 60 protrusions, with the footprint for the AAV5 antibody extending toward the 5-fold axis. The angle of incidence for each bound Fab on the AAVs varied and resulted in significant differences in how much of each viral capsid surface was occluded beyond the Fab footprints. The AAV-antibody interactions showed a common set of footprints that overlapped some known receptor-binding sites and transduction determinants, thus suggesting potential mechanisms for virus neutralization by the antibodies

Overview of the Alliance for Cellular Signaling

The Alliance for Cellular Signaling is a large-scale collaboration designed to answer global questions about signalling networks. Pathways will be studied intensively in two cells-B lymphocytes (the cells of the immune system) and cardiac myocytes-to facilitate quantitative modelling. One goal is to catalyse complementary research in individual laboratories; to facilitate this, all alliance data are freely available for use by the entire research community.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62977/1/nature01304.pd

Complement lectin pathway activation is associated with COVID-19 disease severity, independent of MBL2 genotype subgroups

IntroductionWhile complement is a contributor to disease severity in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, all three complement pathways might be activated by the virus. Lectin pathway activation occurs through different pattern recognition molecules, including mannan binding lectin (MBL), a protein shown to interact with SARS-CoV-2 proteins. However, the exact role of lectin pathway activation and its key pattern recognition molecule MBL in COVID-19 is still not fully understood.MethodsWe therefore investigated activation of the lectin pathway in two independent cohorts of SARS-CoV-2 infected patients, while also analysing MBL protein levels and potential effects of the six major single nucleotide polymorphisms (SNPs) found in the MBL2 gene on COVID-19 severity and outcome.ResultsWe show that the lectin pathway is activated in acute COVID-19, indicated by the correlation between complement activation product levels of the MASP-1/C1-INH complex (p=0.0011) and C4d (p<0.0001) and COVID-19 severity. Despite this, genetic variations in MBL2 are not associated with susceptibility to SARS-CoV-2 infection or disease outcomes such as mortality and the development of Long COVID.ConclusionIn conclusion, activation of the MBL-LP only plays a minor role in COVID-19 pathogenesis, since no clinically meaningful, consistent associations with disease outcomes were noted

Fast determination of structurally cohesive subgroups in large networks

Structurally cohesive subgroups are a powerful and mathematically rigorous way to characterize network robustness. Their strength lies in the ability to detect strong connections among vertices that not only have no neighbors in common, but that may be distantly separated in the graph. Unfortunately, identifying cohesive subgroups is a computationally intensive problem, which has limited empirical assessments of cohesion to relatively small graphs of at most a few thousand vertices. We describe here an approach that exploits the properties of cliques, k-cores and vertex separators to iteratively reduce the complexity of the graph to the point where standard algorithms can be used to complete the analysis. As a proof of principle, we apply our method to the cohesion analysis of a 29,462-vertex biconnected component extracted from a 128,151-vertex co-authorship data set

Unravelling the signal-transduction network in B lymphocytes

The Alliance for Cellular Signaling has chosen the mouse B lymphocyte as a model system to understand basic principles that govern cellular signalling. Progress to that end has focused initially on establishing a reproducible experimental cell system and characterizing essential signalling responses. Although unravelling this complex network will take years, findings revealed in the interim will prove immensely useful to the scientific community at large