The dual string sigma-model of the SU_q(3) sector

In four-dimensional N=4 super Yang-Mills (SYM) the SU(3) sub-sector spanned by purely holomorphic fields is isomorphic to the corresponding mixed one spanned by both holomorphic and antiholomorphic fields. This is no longer the case when one considers the marginally deformed N=4 SYM. The mixed SU(3) sector marginally deformed by a complex parameter beta, i.e. SU_q(3) with q=e^{2 i\pi\beta}, has been shown to be integrable at one-loop hep-th/0703150, while it is not the case for the corresponding purely holomorphic one. Moreover, the marginally deformed N=4 SYM also has a gravity dual constructed by Lunin and Maldacena in hep-th/0502086. However, the mixed SU_q(3) sector has not been studied from the supergravity point of view. Hence in this note, for the case of purely imaginary marginal $\beta$-deformations, we compute the superstring SU_q(3) \sigma-model in the fast spinning string limit and show that, for rational spinning strings, it reproduces the energy computed via Bethe equations.Comment: 20 page

A self-sustaining endocytic-based loop promotes breast cancer plasticity leading to aggressiveness and pro-metastatic behavior

The subversion of endocytic routes leads to malignant transformation and has been implicated in human cancers. However, there is scarce evidence for genetic alterations of endocytic proteins as causative in high incidence human cancers. Here, we report that Epsin 3 (EPN3) is an oncogene with prognostic and therapeutic relevance in breast cancer. Mechanistically, EPN3 drives breast tumorigenesis by increasing E-cadherin endocytosis, followed by the activation of a \u3b2-catenin/TCF4-dependent partial epithelial-to-mesenchymal transition (EMT), followed by the establishment of a TGF\u3b2-dependent autocrine loop that sustains EMT. EPN3-induced partial EMT is instrumental for the transition from in situ to invasive breast carcinoma, and, accordingly, high EPN3 levels are detected at the invasive front of human breast cancers and independently predict metastatic rather than loco-regional recurrence. Thus, we uncover an endocytic-based mechanism able to generate TGF\u3b2-dependent regulatory loops conferring cellular plasticity and invasive behavior

On String S-matrix, Bound States and TBA

The study of finite J effects for the light-cone AdS superstring by means of the Thermodynamic Bethe Ansatz requires an understanding of a companion 2d theory which we call the mirror model. It is obtained from the original string model by the double Wick rotation. The S-matrices describing the scattering of physical excitations in the string and mirror models are related to each other by an analytic continuation. We show that the unitarity requirement for the mirror S-matrix fixes the S-matrices of both theories essentially uniquely. The resulting string S-matrix S(z_1,z_2) satisfies the generalized unitarity condition and, up to a scalar factor, is a meromorphic function on the elliptic curve associated to each variable z. The double Wick rotation is then accomplished by shifting the variables z by quarter of the imaginary period of the torus. We discuss the apparent bound states of the string and mirror models, and show that depending on a choice of the physical region there are one, two or 2^{M-1} solutions of the M-particle bound state equations sharing the same conserved charges. For very large but finite values of J, most of these solutions, however, exhibit various signs of pathological behavior. In particular, they might receive a finite J correction to their energy which is complex, or the energy correction might exceed corrections arising due to finite J modifications of the Bethe equations thus making the asymptotic Bethe ansatz inapplicable.Comment: 77 pages, 6 figures, v2: the statement about the periodicity condition for mirror fermions corrected; typos corrected; references added, v3: misprints correcte

CADM1 inhibits squamous cell carcinoma progression by reducing STAT3 activity.

Although squamous cell carcinomas (SqCCs) of the lungs, head and neck, oesophagus, and cervix account for up to 30% of cancer deaths, the mechanisms that regulate disease progression remain incompletely understood. Here, we use gene transduction and human tumor xenograft assays to establish that the tumour suppressor Cell adhesion molecule 1 (CADM1) inhibits SqCC proliferation and invasion, processes fundamental to disease progression. We determine that the extracellular domain of CADM1 mediates these effects by forming a complex with HER2 and integrin α6β4 at the cell surface that disrupts downstream STAT3 activity. We subsequently show that treating CADM1 null tumours with the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restoration in preventing SqCC growth and metastases. Overall, this study identifies a novel mechanism by which CADM1 prevents SqCC progression and suggests that screening tumours for loss of CADM1 expression will help identify those patients most likely to benefit from JAK/STAT targeted chemotherapies

Pediatric Systemic Multi-Inflammatory Diseases in Italy During Sars-Cov-2 Epidemic: From Kawasaki Disease To Kawacovid

Introduction: Italy was affected by the SARS-CoV-2 epidemic after its outbreak in China. With a 4-weeks delay after the peak in adults, we observed an abnormal number of patients with characteristics of a multi-inflammatory disease and similarities with Kawasaki Disease (KD). Others reported similar cases, defined PIMS-TS or MIS-C.1,2 Objectives: To better characterize clinical features and treatment response of PIMS-TS and to explore its relationship with KD. Methods: We conducted an observational, retrospective, multicenter study. On April 24th-2020 the Rheumatology Study Group of the Italian Pediatric Society launched a national online survey, to enroll patients diagnosed with KD or with a multisystem inflammatory disease between February 1st 2020 and May 31st. The population was then divided into two different groups: 1) Classical and incomplete KD, named Kawasaki Disease Group (KDG); 2) KD-like multi-inflammatory syndrome, named KawaCOVID (KCG). An expert panel of pediatric rheumatologists re-analyzed every single patient to ensure appropriate classification. Data were collected with an online database. Results: 149 cases were studied, 96 with KDG and 53 with KCG. The two population significantly differed for clinical characteristics (see table 1). Lymphopenia, higher CRP levels, elevated Ferritin and Troponin-T characterized KCG such as lower WBC and platelets (all p values<0,05). KDG received more frequently immunoglobulins (IVIG) and acetylsalicylic acid (ASA) (81,3% vs 66%; p=0.04 and 71,9% vs 43,4%; p=0.001 respectively) as KCG more often received glucocorticoids (56,6% vs 14,6%; p<0.0001). SARS-CoV-2 assay more often resulted positive in KCG than in KDG (75,5% vs 20%; p<0.0001). Short-term follow data on KCG showed minor complications while on KDG a majority of patients had persistence of CAA. Comparing KDG with a KD-Historical Italian cohort (598 patients), no statistical difference was found in terms of clinical manifestations and laboratory data between the two groups Conclusion: Our study would suggest that SARS-CoV-2 infection might determine two distinct inflammatory diseases in children: KD, possibly triggered by SARS-CoV-2, and PIMS-TS. Older age at onset and clinical peculiarities, like the occurrence of myocarditis, characterize this multiinflammatory syndrome. Our patients had an optimal response to treatments and a good outcome, with few complications and no deaths

One-loop spectroscopy of semiclassically quantized strings: bosonic sector

We make a further step in the analytically exact quantization of spinning string states in semiclassical approximation, by evaluating the exact one-loop partition function for a class of two-spin string solutions for which quadratic fluctuations form a non-trivial system of coupled modes. This is the case of a folded string in the SU(2) sector, in the limit described by a quantum Landau–Lifshitz model. The same applies to the full bosonic sector of fluctuations over the folded spinning string in AdS5 with an angular momentum J in S5. Fluctuations are governed by a special class of fourth-order differential operators, with coefficients being meromorphic functions on the torus, which we are able to solve exactly

Generalized cusp in AdS_4 x CP^3 and more one-loop results from semiclassical strings

We evaluate the exact one-loop partition function for fundamental strings whose world-surface ends on a cusp at the boundary of AdS_4 and has a "jump" in CP^3. This allows us to extract the stringy prediction for the ABJM generalized cusp anomalous dimension Gamma_{cusp}^{ABJM} (phi,theta) up to NLO in sigma-model perturbation theory. With a similar analysis, we present the exact partition functions for folded closed string solutions moving in the AdS_3 parts of AdS_4 x CP^3 and AdS_3 x S^3 x S^3 x S^1 backgrounds. Results are obtained applying to the string solutions relevant for the AdS_4/CFT_3 and AdS_3/CFT_2 correspondence the tools previously developed for their AdS_5 x S^5 counterparts.Comment: 48 pages, 2 figures, version 3, corrected misprints in formulas 2.12, B.86, C.33, added comment on verification of the light-like limi

Lung adenocarcinoma originates from retrovirus infection of proliferating type 2 pneumocytes during pulmonary post-natal development or tissue repair

Jaagsiekte sheep retrovirus (JSRV) is a unique oncogenic virus with distinctive biological properties. JSRV is the only virus causing a naturally occurring lung cancer (ovine pulmonary adenocarcinoma, OPA) and possessing a major structural protein that functions as a dominant oncoprotein. Lung cancer is the major cause of death among cancer patients. OPA can be an extremely useful animal model in order to identify the cells originating lung adenocarcinoma and to study the early events of pulmonary carcinogenesis. In this study, we demonstrated that lung adenocarcinoma in sheep originates from infection and transformation of proliferating type 2 pneumocytes (termed here lung alveolar proliferating cells, LAPCs). We excluded that OPA originates from a bronchioalveolar stem cell, or from mature post-mitotic type 2 pneumocytes or from either proliferating or non-proliferating Clara cells. We show that young animals possess abundant LAPCs and are highly susceptible to JSRV infection and transformation. On the contrary, healthy adult sheep, which are normally resistant to experimental OPA induction, exhibit a relatively low number of LAPCs and are resistant to JSRV infection of the respiratory epithelium. Importantly, induction of lung injury increased dramatically the number of LAPCs in adult sheep and rendered these animals fully susceptible to JSRV infection and transformation. Furthermore, we show that JSRV preferentially infects actively dividing cell in vitro. Overall, our study provides unique insights into pulmonary biology and carcinogenesis and suggests that JSRV and its host have reached an evolutionary equilibrium in which productive infection (and transformation) can occur only in cells that are scarce for most of the lifespan of the sheep. Our data also indicate that, at least in this model, inflammation can predispose to retroviral infection and cancer