COMBINATORIAL INSCRIBABILITY OBSTRUCTIONS FOR HIGHER DIMENSIONAL POLYTOPES

For 3-dimensional convex polytopes, inscribability is a classical property that is relatively well-understood due to its relation with Delaunay subdivisions of the plane and hyperbolic geometry. In particular, inscribability can be tested in polynomial time, and for every f-vector of 3-polytopes, there exists an inscribable polytope with that f-vector. For higher dimensional polytopes, much less is known. Of course, for any inscribable polytope, all of its lower dimensional faces need to be inscribable, but this condition does not appear to be very strong. We observe non-trivial new obstructions to the inscribability of polytopes that arise when imposing that a certain inscribable face be inscribed. Using this obstruction, we show that the duals of the 4-dimensional cyclic polytopes with at least eight vertices - all of whose faces are inscribable - are not inscribable. This result is optimal in the following sense: We prove that the duals of the cyclic 4-polytopes with up to seven vertices are, in fact, inscribable. Moreover, we interpret this obstruction combinatorially as a forbidden subposet of the face lattice of a polytope, show that d-dimensional cyclic polytopes with at least d+4 vertices are not circumscribable, and that no dual of a neighborly 4-polytope with eight vertices, that is, no polytope with f-vector (20,40,28,8), is inscribable

Combinatorial 3-manifolds with transitive cyclic symmetry

In this article we give combinatorial criteria to decide whether a transitive cyclic combinatorial d-manifold can be generalized to an infinite family of such complexes, together with an explicit construction in the case that such a family exists. In addition, we substantially extend the classification of combinatorial 3-manifolds with transitive cyclic symmetry up to 22 vertices. Finally, a combination of these results is used to describe new infinite families of transitive cyclic combinatorial manifolds and in particular a family of neighborly combinatorial lens spaces of infinitely many distinct topological types.Comment: 24 pages, 5 figures. Journal-ref: Discrete and Computational Geometry, 51(2):394-426, 201

α-Synuclein in human cerebrospinal fluid is principally derived from neurons of the central nervous system

The source of Parkinson disease-linked α-synuclein (aSyn) in human cerebrospinal fluid (CSF) remains unknown. We decided to measure the concentration of aSyn and its gradient in human CSF specimens and compared it with serum to explore its origin. We correlated aSyn concentrations in CSF versus serum (QaSyn) to the albumin quotient (Qalbumin) to evaluate its relation to blood–CSF barrier function. We also compared aSyn with several other CSF constituents of either central or peripheral sources (or both) including albumin, neuron-specific enolase, β-trace protein and total protein content. Finally, we examined whether aSyn is present within the structures of the choroid plexus (CP). We observed that QaSyn did not rise or fall with Qalbumin values, a relative measure of blood–CSF barrier integrity. In our CSF gradient analyses, aSyn levels decreased slightly from rostral to caudal fractions, in parallel to the recorded changes for neuron-specific enolase; the opposite trend was recorded for total protein, albumin and β-trace protein. The latter showed higher concentrations in caudal CSF fractions due to the diffusion-mediated transfer of proteins from blood and leptomeninges into CSF in the lower regions of the spine. In postmortem sections of human brain, we detected highly variable aSyn reactivity within the epithelial cell layer of CP in patients diagnosed with a range of neurological diseases; however, in sections of mice that express only human SNCA alleles (and in those without any Snca gene expression), we detected no aSyn signal in the epithelial cells of the CP. We conclude from these complementary results that despite its higher levels in peripheral blood products, neurons of the brain and spinal cord represent the principal source of aSyn in human CSF

Circulating Pneumolysin Is a Potent Inducer of Cardiac Injury during Pneumococcal Infection

Streptococcus pneumoniae accounts for more deaths worldwide than any other single pathogen through diverse disease manifestations including pneumonia, sepsis and meningitis. Life-threatening acute cardiac complications are more common in pneumococcal infection compared to other bacterial infections. Distinctively, these arise despite effective antibiotic therapy. Here, we describe a novel mechanism of myocardial injury, which is triggered and sustained by circulating pneumolysin (PLY). Using a mouse model of invasive pneumococcal disease (IPD), we demonstrate that wild type PLY-expressing pneumococci but not PLY-deficient mutants induced elevation of circulating cardiac troponins (cTns), well-recognized biomarkers of cardiac injury. Furthermore, elevated cTn levels linearly correlated with pneumococcal blood counts (r=0.688, p=0.001) and levels were significantly higher in non-surviving than in surviving mice. These cTn levels were significantly reduced by administration of PLY-sequestering liposomes. Intravenous injection of purified PLY, but not a non-pore forming mutant (PdB), induced substantial increase in cardiac troponins to suggest that the pore-forming activity of circulating PLY is essential for myocardial injury in vivo. Purified PLY and PLY-expressing pneumococci also caused myocardial inflammatory changes but apoptosis was not detected. Exposure of cultured cardiomyocytes to PLY-expressing pneumococci caused dose-dependent cardiomyocyte contractile dysfunction and death, which was exacerbated by further PLY release following antibiotic treatment. We found that high PLY doses induced extensive cardiomyocyte lysis, but more interestingly, sub-lytic PLY concentrations triggered profound calcium influx and overload with subsequent membrane depolarization and progressive reduction in intracellular calcium transient amplitude, a key determinant of contractile force. This was coupled to activation of signalling pathways commonly associated with cardiac dysfunction in clinical and experimental sepsis and ultimately resulted in depressed cardiomyocyte contractile performance along with rhythm disturbance. Our study proposes a detailed molecular mechanism of pneumococcal toxin-induced cardiac injury and highlights the major translational potential of targeting circulating PLY to protect against cardiac complications during pneumococcal infections

Augmenting the Eye of the Beholder: Exploring the Strategic Potential of Augmented Reality to Enhance Online Service Experiences

Driven by the proliferation of augmented reality (AR) technologies, many firms are pursuing a strategy of service augmentation to enhance customers’ online service experiences. Drawing on situated cognition theory, the authors show that AR - based service augmentation enhances customer value perceptions by simultaneously providing simulated physical control and environmental embedding. The resulting authentic situated experience, manifested in a feeling of spatial presence, funct ions as a mediator and also predicts customer decision comfort. Furthermore, the effect of spatial presence on utilitarian value perceptions is greater for customers who are disposed toward verbal rather than visual information processing, and the positive effect on decision comfort is attenuated by customers’ privacy concerns