Form-factors of the sausage model obtained with bootstrap fusion from sine-Gordon theory

We continue the investigation of massive integrable models by means of the bootstrap fusion procedure, started in our previous work on O(3) nonlinear sigma model. Using the analogy with SU(2) Thirring model and the O(3) nonlinear sigma model we prove a similar relation between sine-Gordon theory and a one-parameter deformation of the O(3) sigma model, the sausage model. This allows us to write down a free field representation for the Zamolodchikov-Faddeev algebra of the sausage model and to construct an integral representation for the generating functions of form-factors in this theory. We also clear up the origin of the singularities in the bootstrap construction and the reason for the problem with the kinematical poles.Comment: 16 pages, revtex; references added, some typos corrected. Accepted for publication in Physical Review

Form factors in the Bullough-Dodd related models: The Ising model in a magnetic field

We consider particular modification of the free-field representation of the form factors in the Bullough-Dodd model. The two-particles minimal form factors are excluded from the construction. As a consequence, we obtain convenient representation for the multi-particle form factors, establish recurrence relations between them and study their properties. The proposed construction is used to obtain the free-field representation of the lightest particles form factors in the $\Phi_{1,2}$ perturbed minimal models. As a significant example we consider the Ising model in a magnetic field. We check that the results obtained in the framework of the proposed free-field representation are in agreement with the corresponding results obtained by solving the bootstrap equations.Comment: 20 pages; v2: some misprints, textual inaccuracies and references corrected; some references and remarks adde

Exact S-matrices for supersymmetric sigma models and the Potts model

We study the algebraic formulation of exact factorizable S-matrices for integrable two-dimensional field theories. We show that different formulations of the S-matrices for the Potts field theory are essentially equivalent, in the sense that they can be expressed in the same way as elements of the Temperley-Lieb algebra, in various representations. This enables us to construct the S-matrices for certain nonlinear sigma models that are invariant under the Lie ``supersymmetry'' algebras sl(m+n|n) (m=1,2; n>0), both for the bulk and for the boundary, simply by using another representation of the same algebra. These S-matrices represent the perturbation of the conformal theory at theta=pi by a small change in the topological angle theta. The m=1, n=1 theory has applications to the spin quantum Hall transition in disordered fermion systems. We also find S-matrices describing the flow from weak to strong coupling, both for theta=0 and theta=pi, in certain other supersymmetric sigma models.Comment: 32 pages, 8 figure

MAIA, Fc receptor–like 3, supersedes JUNO as IZUMO1 receptor during human fertilization

Gamete fusion is a critical event of mammalian fertilization. A random one-bead one-compound combinatorial peptide library represented synthetic human egg mimics and identified a previously unidentified ligand as Fc receptor–like 3, named MAIA after the mythological goddess intertwined with JUNO. This immunoglobulin super family receptor was expressed on human oolemma and played a major role during sperm-egg adhesion and fusion. MAIA forms a highly stable interaction with the known IZUMO1/JUNO sperm-egg complex, permitting specific gamete fusion. The complexity of the MAIA isotype may offer a cryptic sexual selection mechanism to avoid genetic incompatibility and achieve favorable fitness outcomes

A genome-wide association study of anorexia nervosa.

Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countries (15 sites) and 14 860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery data sets. Seventy-six (72 independent) single nucleotide polymorphisms were taken forward for in silico (two data sets) or de novo (13 data sets) replication genotyping in 2677 independent AN cases and 8629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication data sets comprised 5551 AN cases and 21 080 controls. AN subtype analyses (1606 AN restricting; 1445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01 × 10(-7)) in SOX2OT and rs17030795 (P=5.84 × 10(-6)) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76 × 10(-)(6)) between CUL3 and FAM124B and rs1886797 (P=8.05 × 10(-)(6)) near SPATA13. Comparing discovery with replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P=4 × 10(-6)), strongly suggesting that true findings exist but our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field

A genome-wide association study of anorexia nervosa

Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2,907 cases with AN from 14 countries (15 sites) and 14,860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery datasets. Seventy-six (72 independent) SNPs were taken forward for in silico (two datasets) or de novo (13 datasets) replication genotyping in 2,677 independent AN cases and 8,629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication datasets comprised 5,551 AN cases and 21,080 controls. AN subtype analyses (1,606 AN restricting; 1,445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01×10−7) in SOX2OT and rs17030795 (P=5.84×10−6) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76×10−6) between CUL3 and FAM124B and rs1886797 (P=8.05×10−6) near SPATA13. Comparing discovery to replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P= 4×10−6), strongly suggesting that true findings exist but that our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field

A genome-wide association study of anorexia nervosa suggests a risk locus implicated in dysregulated leptin signaling

J. Kaprio, A. Palotie, A. Raevuori-Helkamaa ja S. Ripatti ovat työryhmän Eating Disorders Working Group of the Psychiatric Genomics Consortium jäseniä. Erratum in: Sci Rep. 2017 Aug 21;7(1):8379, doi: 10.1038/s41598-017-06409-3We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenotype. Analysis of phenotypic variability led to the identification of a specific genetic risk factor that approached genome-wide significance (rs929626 in EBF1 (Early B-Cell Factor 1); P = 2.04 x 10(-7); OR = 0.7; 95% confidence interval (CI) = 0.61-0.8) with independent replication (P = 0.04), suggesting a variant-mediated dysregulation of leptin signaling may play a role in AN. Multiple SNPs in LD with the variant support the nominal association. This demonstrates that although the clinical and etiologic heterogeneity of AN is universally recognized, further careful sub-typing of cases may provide more precise genomic signals. In this study, through a refinement of the phenotype spectrum of AN, we present a replicable GWAS signal that is nominally associated with AN, highlighting a potentially important candidate locus for further investigation.Peer reviewe