BRST cohomology of timelike Liouville theory

We compute the Hermitian sector of the relative BRST cohomology of the spacelike and timelike Liouville theories with generic real central charge $c_L$ in each case, coupled to a spacelike Coulomb gas and a generic transverse CFT. This paper is a companion of arXiv:1905.12689, and its main goal is to completely characterize the cohomology of the timelike theory with $c_L 1$, which includes generalized minimal gravity. We prove a no-ghost theorem for the Hermitian sector in the timelike theory and for some spacelike models

Two and four-loop β\beta-functions of rank 4 renormalizable tensor field theories

A recent rank 4 tensor field model generating 4D simplicial manifolds has been proved to be renormalizable at all orders of perturbation theory [arXiv:1111.4997 [hep-th]]. The model is built out of $\phi^6$ ($\phi^6_{(1/2)}$), $\phi^4$ ($\phi^4_{(1)}$) interactions and an anomalous term ($\phi^4_{(2)}$). The $\beta$-functions of this model are evaluated at two and four loops. We find that the model is asymptotically free in the UV for both the main $\phi^6_{(1/2)}$ interactions whereas it is safe in the $\phi^4_{(1)}$ sector. The remaining anomalous term turns out to possess a Landau ghost.Comment: 31 pages, 31 figures; improved versio

Identification of myxomaviral serpin reactive site loop sequences that regulate innate immune responses.

The thrombolytic serine protease cascade is intricately involved in activation of innate immune responses. The urokinase-type plasminogen activator and receptor form complexes that aid inflammatory cell invasion at sites of arterial injury. Plasminogen activator inhibitor-1 is a mammalian serpin that binds and regulates the urokinase receptor complex. Serp-1, a myxomaviral serpin, also targets the urokinase receptor, displaying profound anti-inflammatory and anti-atherogenic activity in a wide range of animal models. Serp-1 reactive center site mutations, mimicking known mammalian and viral serpins, were constructed in order to define sequences responsible for regulation of inflammation. Thrombosis, inflammation, and plaque growth were assessed after treatment with Serp-1, Serp-1 chimeras, plasminogen activator inhibitor-1, or unrelated viral serpins in plasminogen activator inhibitor or urokinase receptor-deficient mouse aortic transplants. Altering the P1-P1\u27 Arg-Asn sequence compromised Serp-1 protease-inhibitory activity and anti-inflammatory activity in animal models; P1-P1\u27 Ala-Ala mutants were inactive, P1 Met increased remodeling, and P1\u27 Thr increased thrombosis. Substitution of Serp-1 P2-P7 with Ala6 allowed for inhibition of urokinase but lost plasmin inhibition, unexpectedly inducing a diametrically opposed, proinflammatory response with mononuclear cell activation, thrombosis, and aneurysm formation (p \u3c 0.03). Other serpins did not reproduce Serp-1 activity; plasminogen activator inhibitor-1 increased thrombosis (p \u3c 0.0001), and unrelated viral serpin, CrmA, increased inflammation. Deficiency of urokinase receptor in mouse transplants blocked Serp-1 and chimera activity, in some cases increasing inflammation. In summary, 1) Serp-1 anti-inflammatory activity is highly dependent upon the reactive center loop sequence, and 2) plasmin inhibition is central to anti-inflammatory activity