Generating all permutations by context-free grammars in Chomsky normal form

Let Ln be the finite language of all n! strings that are permutations of n different symbols (n1). We consider context-free grammars Gn in Chomsky normal form that generate Ln. In particular we study a few families {Gn}n1, satisfying L(Gn)=Ln for n1, with respect to their descriptional complexity, i.e. we determine the number of nonterminal symbols and the number of production rules of Gn as functions of n

The aspherical Cavicchioli-Hegenbarth-Repovš generalized Fibonacci groups

The Cavicchioli–Hegenbarth–Repovš generalized Fibonacci groups are defined by the presentations Gn (m, k) = 〈x 1, … , xn | xixi+m = xi+k (1 ⩽ i ⩽ n)〉. These cyclically presented groups generalize Conway's Fibonacci groups and the Sieradski groups. Building on a theorem of Bardakov and Vesnin we classify the aspherical presentations Gn (m, k). We determine when Gn (m, k) has infinite abelianization and provide sufficient conditions for Gn (m, k) to be perfect. We conjecture that these are also necessary conditions. Combined with our asphericity theorem, a proof of this conjecture would imply a classification of the finite Cavicchioli–Hegenbarth–Repovš groups

Possible Magnetic Chirality in Optically Chiral Magnet [Cr(CN)6_6][Mn(SS)-pnH(H2_2O)](H2_2O) Probed by Muon Spin Rotation and Relaxation

Local magnetic fields in a molecule-based optically chiral magnet [Cr(CN)$_6$][Mn($S$)-pnH(H$_2$O)](H$_2$O) (GN-S) and its enantiomer (GN-R) are studied by means of muon spin rotation and relaxation (muSR). Detailed analysis of muon precession signals under zero field observed below T_c supports the average magnetic structure suggested by neutron powder diffraction. Moreover, comparison of muSR spectra between GN-S and GN-R suggests that they are a pair of complete optical isomers in terms of both crystallographic and magnetic structure. Possibility of magnetic chirality in such a pair is discussed.Comment: 5 pages, 5 figures, submitted to J. Phys. Soc. Jp

Vaccination with DNA plasmids expressing Gn coupled to C3d or alphavirus replicons expressing Gn protects mice against rift valley fever virus

Background: Rift Valley fever (RVF) is an arthropod-borne viral zoonosis. Rift Valley fever virus (RVFV) is an important biological threat with the potential to spread to new susceptible areas. In addition, it is a potential biowarfare agent. Methodology/Principal Findings: We developed two potential vaccines, DNA plasmids and alphavirus replicons, expressing the Gn glycoprotein of RVFV alone or fused to three copies of complement protein, C3d. Each vaccine was administered to mice in an all DNA, all replicon, or a DNA prime/replicon boost strategy and both the humoral and cellular responses were assessed. DNA plasmids expressing Gn-C3d and alphavirus replicons expressing Gn elicited high titer neutralizing antibodies that were similar to titers elicited by the live-attenuated MP12 virus. Mice vaccinated with an inactivated form of MP12 did elicit high titer antibodies, but these antibodies were unable to neutralize RVFV infection. However, only vaccine strategies incorporating alphavirus replicons elicited cellular responses to Gn. Both vaccines strategies completely prevented weight loss and morbidity and protected against lethal RVFV challenge. Passive transfer of antisera from vaccinated mice into naïve mice showed that both DNA plasmids expressing Gn-C3d and alphavirus replicons expressing Gn elicited antibodies that protected mice as well as sera from mice immunized with MP12. Conclusion/Significance: These results show that both DNA plasmids expressing Gn-C3d and alphavirus replicons expressing Gn administered alone or in a DNA prime/replicon boost strategy are effective RVFV vaccines. These vaccine strategies provide safer alternatives to using live-attenuated RVFV vaccines for human use. © 2010 Bhardwaj et al

Protease-activated receptor 1 mediates thrombin-dependent, cell-mediated renal inflammation in crescentic glomerulonephritis.

Protease-activated receptor (PAR)-1 is a cellular receptor for thrombin that is activated after proteolytic cleavage. The contribution of PAR-1 to inflammatory cell-mediated renal injury was assessed in murine crescentic glomerulonephritis (GN). A pivotal role for thrombin in this model was demonstrated by the capacity of hirudin, a selective thrombin antagonist, to attenuate renal injury. Compared with control treatment, hirudin significantly reduced glomerular crescent formation, T cell and macrophage infiltration, fibrin deposition, and elevated serum creatinine, which are prominent features of GN. PAR-1-deficient (PAR-1(-/-)) mice, which have normal coagulation, also showed significant protection from crescentic GN compared with wild-type mice. The reductions in crescent formation, inflammatory cell infiltration, and serum creatinine were similar in PAR-1(-/-) and hirudin-treated mice, but hirudin afforded significantly greater protection from fibrin deposition. Treatment of wild-type mice with a selective PAR-1-activating peptide (TRAP) augmented histological and functional indices of GN, but TRAP treatment did not alter the severity of GN in PAR(-/-) mice. These results indicate that activation of PAR-1 by thrombin or TRAP amplifies crescentic GN. Thus, in addition to its procoagulant role, thrombin has proinflammatory, PAR-1-dependent effects that augment inflammatory renal injury