Vertex-Unfoldings of Simplicial Polyhedra

We present two algorithms for unfolding the surface of any polyhedron, all of whose faces are triangles, to a nonoverlapping, connected planar layout. The surface is cut only along polyhedron edges. The layout is connected, but it may have a disconnected interior: the triangles are connected at vertices, but not necessarily joined along edges.Comment: 10 pages; 7 figures; 8 reference

Mott transition in the π\pi-flux SU(44) Hubbard model on a square lattice

We employ the projector quantum Monte Carlo simulations to study the ground-state properties of the square-lattice SU(4) Hubbard model with a $\pi$ flux per plaquette. In the weak coupling regime, its ground state is in the gapless Dirac semi-metal phase. With increasing repulsive interaction, we show that, a Mott transition occurs from the semimetal to the valence bond solid, accompanied by the $Z_4$ discrete symmetry breaking. Our simulations demonstrate the existence of a second-order phase transition, which confirms the Ginzburg-Landau analysis. The phase transition point and the critical exponent $\eta$ are also estimated. To account for the effect of a $\pi$ flux on the ordering in the strong coupling regime, we analytically derive by the perturbation theory the ring-exchange term which describes the leading-order difference between the $\pi$-flux and zero-flux SU(4) Hubbard models.Comment: 8 pages, 9 figure

Beneficial hemodynamic effects of intravenous and oral diltiazem in severe congestive heart failure

Concern persists about the potential negative inotropic effects of calcium channel blockers in patients with severely depressed myocardial function. Therefore, intravenous diltiazem (100 to 200 ltg/kg per min infusion) was administered for 40 minutes followed by oral diltiazem (90 to 120 mg/8 hours) for 24 hours to patients with advanced congestive heart failure (New York Heart Association class III to IV, mean ejection fraction 26 ± 4 [SD]). Intravenous diltiazem (eight patients) increased cardiac index 20% (2.05 ± 0.8 to 2.47 ± 0.8 liters/min per MZ, p < 0.01), stroke volume index 50% (22 ± 9 to 33 ± 12 MI/M2, p < 0.001) and stroke work index 27% (19 ± 10 to 24 ± 10 g-m/MZ, p < 0.05); while reducing heart rate 23% (97 ± 18 to 75 ± 11 beats/min, p < 0.01), mean arterial pressure 18% (95 ± 13 to 78 ± 7 mm Hg) and pulmonary wedge pressure 34% (29 ± 9 to 19 ± 7 mm Hg), without altering maximal first derivative of left ventricular pressure (dP/dtmax). Oral diltiazem (seven patients) produced equivalent hemodynamic effects. Transient junctional arrhythmias were observed in three of eight patients with intravenous diltiazem and one of seven patients with oral diltiazem.It is concluded that intravenous and short-term oral diltiazem improve left ventricular performance and reduce myocardial oxygen demand by heart rate and afterload reduction without significantly depressing contractile function in severe congestive heart failure. Caution should be exercised to avoid potential adverse, druginduced electrophysiologic effects in such patients

Microscopic biophysical model of self-organization in tissue due to feedback between cell- and macroscopic-scale forces

We develop a microscopic biophysical model for self-organization and reshaping of artificial tissue, that is codriven by microscopic active forces between cells and an extracellular matrix (ECM), and macroscopic forces that develop within the tissue, finding close agreement with experiment. Microscopic active forces are stimulated by μm-scale interactions between cells and the ECM within which they exist, and when large numbers of cells act together these forces drive, and are affected by, macroscopic-scale self-organization and reshaping of tissues in a feedback loop. To understand this loop, there is a need to (1) construct microscopic biophysical models that can simulate these processes for the very large number of cells found in tissues, (2) validate and calibrate those models against experimental data, and (3) understand the active feedback between cells and the extracellular matrix, and its relationship to macroscopic self-organization and reshaping of tissue. Our microscopic biophysical model consists of a contractile network representing the ECM, that interacts with a large number of cells via dipole forces, to describe macroscopic self-organization and reshaping of tissue. We solve the model using simulated annealing, finding close agreement with experiments on artificial neural tissue. We discuss the calibration of model parameters. We conclude that feedback between microscopic cell-ECM dipole interactions and tissue-scale forces is a key factor in driving macroscopic self-organization and reshaping of tissue. We discuss the application of the biophysical model to the simulation and rational design of artificial tissues

Whole-Genome Sequencing and Concordance Between Antimicrobial Susceptibility Genotypes and Phenotypes of Bacterial Isolates Associated with Bovine Respiratory Disease.

Extended laboratory culture and antimicrobial susceptibility testing timelines hinder rapid species identification and susceptibility profiling of bacterial pathogens associated with bovine respiratory disease, the most prevalent cause of cattle mortality in the United States. Whole-genome sequencing offers a culture-independent alternative to current bacterial identification methods, but requires a library of bacterial reference genomes for comparison. To contribute new bacterial genome assemblies and evaluate genetic diversity and variation in antimicrobial resistance genotypes, whole-genome sequencing was performed on bovine respiratory disease-associated bacterial isolates (Histophilus somni, Mycoplasma bovis, Mannheimia haemolytica, and Pasteurella multocida) from dairy and beef cattle. One hundred genomically distinct assemblies were added to the NCBI database, doubling the available genomic sequences for these four species. Computer-based methods identified 11 predicted antimicrobial resistance genes in three species, with none being detected in M. bovis While computer-based analysis can identify antibiotic resistance genes within whole-genome sequences (genotype), it may not predict the actual antimicrobial resistance observed in a living organism (phenotype). Antimicrobial susceptibility testing on 64 H. somni, M. haemolytica, and P. multocida isolates had an overall concordance rate between genotype and phenotypic resistance to the associated class of antimicrobials of 72.7% (P &lt; 0.001), showing substantial discordance. Concordance rates varied greatly among different antimicrobial, antibiotic resistance gene, and bacterial species combinations. This suggests that antimicrobial susceptibility phenotypes are needed to complement genomically predicted antibiotic resistance gene genotypes to better understand how the presence of antibiotic resistance genes within a given bacterial species could potentially impact optimal bovine respiratory disease treatment and morbidity/mortality outcomes