Once again on the equivalence theorem

We present the proof of the equivalence theorem in quantum field theory which is based on a formulation of this problem in the field-antifield formalism. As an example, we consider a model in which a different choices of natural finite counterterms is possible, leading to physically non-equivalent quantum theories while the equivalent theorem remains valid.Comment: 12 pages, LATEX, report number was correcte

Initial Conditions for Semiclassical Field Theory

Semiclassical approximation based on extracting a c-number classical component from quantum field is widely used in the quantum field theory. Semiclassical states are considered then as Gaussian wave packets in the functional Schrodinger representation and as Gaussian vectors in the Fock representation. We consider the problem of divergences and renormalization in the semiclassical field theory in the Hamiltonian formulation. Although divergences in quantum field theory are usually associated with loop Feynman graphs, divergences in the Hamiltonian approach may arise even at the tree level. For example, formally calculated probability of pair creation in the leading order of the semiclassical expansion may be divergent. This observation was interpretted as an argumentation for considering non-unitary evolution transformations, as well as non-equivalent representations of canonical commutation relations at different time moments. However, we show that this difficulty can be overcomed without the assumption about non-unitary evolution. We consider first the Schrodinger equation for the regularized field theory with ultraviolet and infrared cutoffs. We study the problem of making a limit to the local theory. To consider such a limit, one should impose not only the requirement on the counterterms entering to the quantum Hamiltonian but also the requirement on the initial state in the theory with cutoffs. We find such a requirement in the leading order of the semiclassical expansion and show that it is invariant under time evolution. This requirement is also presented as a condition on the quadratic form entering to the Gaussian state.Comment: 20 pages, Plain TeX, one postscript figur

Structural Insight into Archaic and Alternative Chaperone-Usher Pathways Reveals a Novel Mechanism of Pilus Biogenesis

AVZ is supported by the Finnish Academy (grants 140959 and 273075; http://sciencenordic.com/partner/academy-finland) and Sigrid Juselius Foundation (grant 2014; www.sigridjuselius.fi/foundation). SMis supported by the Wellcome Trust (Senior Investigator Award 100280, Programme grant 079819; http://www.wellcome.ac.uk) The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Cell Membrane Is Impaired, Accompanied by Enhanced Type III Secretion System Expression in Yersinia pestis Deficient in RovA Regulator

BACKGROUND: In the enteropathogenic Yersinia species, RovA regulates the expression of invasin, which is important for enteropathogenic pathogenesis but is inactivated in Yersinia pestis. Investigation of the RovA regulon in Y. pestis at 26 °C has revealed that RovA is a global regulator that contributes to virulence in part by the direct regulation of psaEFABC. However, the regulatory roles of RovA in Y. pestis at 37 °C, which allows most virulence factors in mammalian hosts to be expressed, are still poorly understood. METHODOLOGY/PRINCIPAL FINDINGS: The transcriptional profile of an in-frame rovA mutant of Y. pestis biovar Microtus strain 201 was analyzed under type III secretion system (T3SS) induction conditions using microarray techniques, and it was revealed that many cell-envelope and transport/binding proteins were differentially expressed in the ΔrovA mutant. Most noticeably, many of the T3SS genes, including operons encoding the translocon, needle and Yop (Yersinia outer protein) effectors, were significantly up-regulated. Analysis of Yop proteins confirmed that YopE and YopJ were also expressed in greater amounts in the mutant. However, electrophoresis mobility shift assay results demonstrated that the His-RovA protein could not bind to the promoter sequences of the T3SS genes, suggesting that an indirect regulatory mechanism is involved. Transmission electron microscopy analysis indicated that there are small loose electron dense particle-like structures that surround the outer membrane of the mutant cells. The bacterial membrane permeability to CFSE (carboxyfluorescein diacetate succinimidyl ester) was significantly decreased in the ΔrovA mutant compared to the wild-type strain. Taken together, these results revealed the improper construction and dysfunction of the membrane in the ΔrovA mutant. CONCLUSIONS/SIGNIFICANCE: We demonstrated that the RovA regulator plays critical roles in the construction and functioning of the bacterial membrane, which sheds considerable light on the regulatory functions of RovA in antibiotic resistance and environmental adaptation. The expression of T3SS was upregulated in the ΔrovA mutant through an indirect regulatory mechanism, which is possibly related to the altered membrane construction in the mutant

Caf1R gene and its role in the regulation of capsule formation of Y. pestis.

AbstractA new transcription unit of the f1 gene cluster was found. The DNA sequencing revealed one long open reading frame. Deletion and frame shift mutation analyses have demonstrated the importance of a corresponding gene product for the F1 antigen biosynthesis. A homology of the deduced amino acid sequence with that of AraC family DNA-binding regulators was shown. A potential regulatory DNA region is discussed