Gluon Radiation and Coherent States in Ultrarelativistic Nuclear Collisions

We explore the correspondence between classical gluon radiation and quantum radiation in a coherent state for gluons produced in ultrarelativistic nuclear collisions. The expectation value of the invariant momentum distribution of gluons in the coherent state is found to agree with the gluon number distribution obtained classically from the solution of the Yang-Mills equations. A criterion for the applicability of the coherent state formalism to the problem of radiation in ultrarelativistic nucleus-nucleus collisions is discussed. This criterion is found to be fulfilled for midrapidity gluons with perturbative transverse momenta larger than about 1-2 GeV and produced in collisions between valence partons.Comment: 15 pages, 6 figures, RevTeX (with epsf, psfig style files

Classical Gluon Radiation in Ultrarelativistic Nuclear Collisions: Space-Time Structure, Instabilities, and Thermalization

We investigate the space-time structure of the classical gluon field produced in an ultrarelativistic collision between color charges. The classical solution which was computed previously in a perturbative approach is shown to become unstable on account of the non-Abelian self-interaction neglected in the perturbative solution scheme. The time scale for growth of the instabilities is found to be of the order of the distance between the colliding color charges. We argue that these instabilities will eventually lead to thermalization of gluons produced in an ultrarelativistic collision between heavy nuclei. The rate of thermalization is estimated to be of order $g^2 \mu$, where $g$ is the strong coupling constant and $\mu^2$ the transverse color charge density of an ultrarelativistic nucleus.Comment: 11 pages, REVTeX, eps-, aps-, and psfig-style files, 7 figs., figs. 2-5 in gif-format, a uucompressed version of this paper including all figures (ca. 2.2 Mb) is available at ftp://nt1.phys.columbia.edu/pub/stabil/stab.u

Mutations in epigenetic regulators including SETD2 are gained during relapse in pediatric acute lymphoblastic leukemia

Relapsed pediatric acute lymphoblastic leukemia (ALL) has high rates of treatment failure. Epigenetic regulators have been proposed as modulators of chemoresistance, here we sequence genes encoding epigenetic regulators in matched diagnosis-remission-relapse ALL samples. We find significant enrichment of mutations in epigenetic regulators at relapse with recurrent somatic mutations in SETD2, CREBBP, MSH6, KDM6A and MLL2, mutations in signaling factors are not enriched. Somatic alterations in SETD2, including frameshift and nonsense mutations, are present at 12% in a large de novo ALL patient cohort. We conclude that the enrichment of mutations in epigenetic regulators at relapse is consistent with a role in mediating therapy resistance

Characterization of a novel fusion gene EML4-NTRK3 in a case of recurrent congenital fibrosarcoma

We describe the clinical course of a recurrent case of congenital fibrosarcoma diagnosed in a 9-mo-old boy with a history of hemimelia. Following complete surgical resection of the primary tumor, the patient subsequently presented with bulky bilateral pulmonary metastases 6 mo following surgery. Molecular characterization of the tumor revealed the absence of the prototypical ETV6-NTRK3 translocation. However, tumor characterization incorporating cytogenetic, array comparative genomic hybridization, and RNA sequencing analyses, revealed a somatic t(2;15)(2p21;15q25) translocation resulting in the novel fusion of EML4 with NTRK3. Cloning and expression of EML4-NTRK3 in murine fibroblast NIH 3T3 cells revealed a potent tumorigenic phenotype as assessed in vitro and in vivo. These results demonstrate that multiple fusion partners targeting NTRK3 can contribute to the development of congenital fibrosarcoma

Self-bias and the emotionality of foreign languages

Article first published online: June 13, 2018Foreign language contexts impose a relative psychological and emotional distance in bilinguals. In our previous studies, we demonstrated that the use of a foreign language changes the strength of the seemingly automatic emotional responses in the self-paradigm, showing a robust asymmetry in the self-bias effect in a native and a foreign language context. Namely, larger effects were found in the native language, suggesting an emotional blunting in the foreign language context. In the present study, we investigated the source of these effects by directly comparing whether they stem from a language’s foreignness versus its non-nativeness. We employed the same self-paradigm (a simple perceptual matching task of associating simple geometric shapes with the labels “you,” “friend,” and “other”), testing unbalanced Spanish–Basque–English trilinguals. We applied the paradigm to three language contexts: native, non-native but contextually present (i.e., non-native local), and non-native foreign. Results showed a smaller self-bias only in the foreign language pointing to the foreign-language-induced psychological/emotional distance as the necessary prerequisite for foreign language effects. Furthermore, we explored whether perceived emotional distance towards foreign languages in Spanish–English bilinguals modulates foreign language effects. Results suggest that none of the different indices of emotional distance towards the foreign language obtained via questionnaires modulated the self-biases in the foreign language contexts. Our results further elucidate the deeply rooted and automatic nature of foreign-language-driven differential emotional processing.This research has been partially funded by grants PSI2015-65689-P and SEV-2015-0490 from the Spanish Government, AThEME-613465 from the European Union, and a 2016 BBVA Foundation Grant for Researchers and Cultural Creators awarded to the last author (J.A.D.)

Use of non-steroidal anti-inflammatory drugs and risk of breast cancer: The Spanish Multi-Case-control (MCC) study

Background: The relationship between non-steroidal anti-inflammatory drug (NSAID) consumption and breast cancer has been repeatedly studied, although the results remain controversial. Most case-control studies reported that NSAID consumption protected against breast cancer, while most cohort studies did not find this effect. Most studies have dealt with NSAIDs as a whole group or with specific drugs, such aspirin, ibuprofen, or others, but not with NSAID subgroups according to the Anatomical Therapeutic Chemical Classification System; moreover, scarce attention has been paid to their effect on different tumor categories (i.e.: ductal/non-ductal, stage at diagnosis or presence of hormonal receptors). Methods: In this case-control study, we report the NSAID – breast cancer relationship in 1736 breast cancer cases and 1895 healthy controls; results are reported stratifying by the women’s characteristics (i.e.: menopausal status or body mass index category) and by tumor characteristics. Results: In our study, NSAID use was associated with a 24 % reduction in breast cancer risk (Odds ratio [OR] = 0.76; 95 % Confidence Interval [CI]: 0.64–0.89), and similar results were found for acetic acid derivatives, propionic acid derivatives and COXIBs, but not for aspirin. Similar results were found in postmenopausal and premenopausal women. NSAID consumption also protected against hormone + or HER2+ cancers, but not against triple negative breast cancers. The COX-2 selectivity showed an inverse association with breast cancer (i.e. OR < 1), except in advanced clinical stage and triple negative cancers. Conclusion: Most NSAIDs, but not aspirin, showed an inverse association against breast cancer; this effect seems to be restricted to hormone + or HER2+ cancers. Keywords: Breast cancer, Non-steroidal anti-inflammatory drug, Hormone receptor positive breast cancer, HER2 positive breast cancer, Triple negative breast cance

Classical Gluon Radiation in Ultrarelativistic Nucleus-Nucleus Collisions

The classical Yang-Mills equations are solved perturbatively in covariant gauge for a collision of two ultrarelativistic nuclei. The nuclei are taken as ensembles of classical color charges on eikonal trajectories. The classical gluon field is computed in coordinate space up to cubic order in the coupling constant g. We construct the Feynman diagrams corresponding to this field and show the equivalence of the classical and diagrammatic approaches. An argument is given which demonstrates that at higher orders in g the classical description of the process breaks down. As an application, we calculate the energy, number, and multiplicity distributions of produced soft gluons and reproduce earlier results by Gunion and Bertsch and by Kovner, McLerran, and Weigert.Comment: 15 pages, REVTeX, 3 figure

Fanconi-BRCA pathway mutations in childhood T-cell acute lymphoblastic leukemia

BRCA2 (also known as FANCD1) is a core component of the Fanconi pathway and suppresses transformation of immature T-cells in mice. However, the contribution of Fanconi-BRCA pathway deficiency to human T-cell acute lymphoblastic leukemia (T-ALL) remains undefined. We identified point mutations in 9 (23%) of 40 human T-ALL cases analyzed, with variant allele fractions consistent with heterozygous mutations early in tumor evolution. Two of these mutations were present in remission bone marrow specimens, suggesting germline alterations. BRCA2 was the most commonly mutated gene. The identified Fanconi-BRCA mutations encode hypomorphic or null alleles, as evidenced by their inability to fully rescue Fanconi-deficient cells from chromosome breakage, cytotoxicity and/or G2/M arrest upon treatment with DNA cross-linking agents. Disabling the tumor suppressor activity of the Fanconi-BRCA pathway is generally thought to require biallelic gene mutations. However, all mutations identified were monoallelic, and most cases appeared to retain expression of the wild-type allele. Using isogenic T-ALL cells, we found that BRCA2 haploinsufficiency induces selective hypersensitivity to ATR inhibition, in vitro and in vivo. These findings implicate Fanconi-BRCA pathway haploinsufficiency in the molecular pathogenesis of T-ALL, and provide a therapeutic rationale for inhibition of ATR or other druggable effectors of homologous recombination