Stochastic differential equations and stochastic parallel translations in the Wasserstein space

We will develop some elements in stochastic analysis in the Wasserstein space $\mathbb{P}_2(M)$ over a compact Riemannian manifold $M$, such as intrinsic It$\^o$ formulae, stochastic regular curves and parallel translations along them. We will establish the existence of parallel translations along regular curves, or stochastic regular curves in case of $\mathbb{P}_2(\mathbb{T})$. Surprisingly enough, in this last case, the equation defining stochastic parallel translations is a SDE on a Hilbert space, instead of a SPDE

A2(2)A^{(2)}_2 Parafermions: A New Conformal Field Theory

A new parafermionic algebra associated with the homogeneous space $A^{(2)}_2/U(1)$ and its corresponding $Z$-algebra have been recently proposed. In this paper, we give a free boson representation of the $A^{(2)}_2$ parafermion algebra in terms of seven free fields. Free field realizations of the parafermionic energy-momentum tensor and screening currents are also obtained. A new algebraic structure is discovered, which contains a $W$-algebra type primary field with spin two.Comment: LaTex 19 pages. Version to appear in Nucl. Phys.

Twisted Parafermions

A new type of nonlocal currents (quasi-particles), which we call twisted parafermions, and its corresponding twisted $Z$-algebra are found. The system consists of one spin-1 bosonic field and six nonlocal fields of fractional spins. Jacobi-type identities for the twisted parafermions are derived, and a new conformal field theory is constructed from these currents. As an application, a parafermionic representation of the twisted affine current algebra $A^{(2)}_2$ is given.Comment: RevTex 5 pages; Cosmetic changes, to appear in Phys.Lett.

Involvement and therapeutic implications of airway epithelial barrier dysfunction in type 2 inflammation of asthma

Type 2 inflammation is a complex immune response and primary mechanism for several common allergic diseases including allergic rhinitis, allergic asthma, atopic dermatitis, and chronic rhinosinusitis with nasal polyps. It is the predominant type of immune response against helminths to prevent their tissue infiltration and induce their expulsion. Recent studies suggest that epithelial barrier dysfunction contributes to the development of type 2 inflammation in asthma, which may partly explain the increasing prevalence of asthma in China and around the globe. The epithelial barrier hypothesis has recently been proposed and has received great interest from the scientific community. The development of leaky epithelial barriers leads to microbial dysbiosis and the translocation of bacteria to inter- and sub-epithelial areas and the development of epithelial tissue inflammation. Accordingly, preventing the impairment and promoting the restoration of a deteriorated airway epithelial barrier represents a promising strategy for the treatment of asthma. This review introduces the interaction between type 2 inflammation and the airway epithelial barrier in asthma, the structure and molecular composition of the airway epithelial barrier, and the assessment of epithelial barrier integrity. The role of airway epithelial barrier disruption in the pathogenesis of asthma will be discussed. In addition, the possible mechanisms underlying the airway epithelial barrier dysfunction induced by allergens and environmental pollutants, and current treatments to restore the airway epithelial barrier are reviewed

1-[(6-Chloro-3-pyrid­yl)meth­yl]-N-(4-ethoxy­phen­yl)-3-phenyl-1H-pyrazole-5-carboxamide

In the title compound, C24H21ClN4O2, the pyrazole ring makes dihedral angles of 7.70 (11), 89.17 (11) and 40.68 (11)° with the phenyl, pyridine and ethoxy­phenyl rings, respectively. There are some intra­molecular C—H⋯O and C—H⋯π bonds giving rigidity to the mol­ecule, while weak inter­molecular N—H⋯N and C—H⋯π hydrogen bonds link the mol­ecules into a two-dimensional structure

A Genome-Wide Association Study Identifies Two Novel Promising Candidate Genes Affecting Escherichia coli F4ab/F4ac Susceptibility in Swine

Enterotoxigenic Escherichia coli (ETEC) expressing F4 fimbria is the major pathogenic bacteria causing diarrhoea in neonatal and post-weaning piglets. Previous studies have revealed that the susceptibility to ETEC F4ab/F4ac is an autosomal Mendelian dominant trait and the loci controlling the F4ab/F4ac receptor are located on SSC13q41, between markers SW207 and S0283. To pinpoint these loci and further validate previous findings, we performed a genome-wide association study (GWAS) using a two generation family-based population, consisting of 301 piglets with phenotypes of susceptibility to ETEC F4ab/F4ac by the vitro adhesion test. The DNA of all piglets and their parents was genotyped using the Illumina PorcineSNP60 BeadChip, and 50,972 and 50,483 SNPs were available for F4ab and F4ac susceptibility, respectively, in the association analysis after quality control. In summary, 28 and 18 significant SNPs (p<0.05) were detected associated with F4ab and F4ac susceptibility respectively at genome-wide significance level. From these significant findings, two novel candidate genes, HEG1 and ITGB5, were firstly identified as the most promising genes underlying F4ab/F4ac susceptibility in swine according to their functions and positions. Our findings herein provide a novel evidence for unravelling genetic mechanism of diarrhoea risk in piglets