Anomaly Cancellation and Conformality in Quiver Gauge Theories

Abelian quiver gauge theories provide nonsupersymmetric candidates for the conformality approach to physics beyond the standard model. Written as ${\cal N}=0$, $U(N)^n$ gauge theories, however, they have mixed $U(1)_p U(1)_q^2$ and $U(1)_p SU(N)_q^2$ triangle anomalies. It is shown how to construct explicitly a compensatory term $\Delta{\cal L}_{comp}$ which restores gauge invariance of ${\cal L}_{eff} = {\cal L} + \Delta {\cal L}_{comp}$ under $U(N)^n$. It can lead to a negative contribution to the U(1) $\beta$-function and hence to one-loop conformality at high energy for all dimensionless couplings.Comment: 15 pages. minor clarification

BMP-7 Does Not Protect against Bleomycin-Induced Lung or Skin Fibrosis

Bone morphogenic protein (BMP)-7 is a member of the BMP family which are structurally and functionally related, and part of the TGFβ super family of growth factors. BMP-7 has been reported to inhibit renal fibrosis and TGFβ1-induced epithelial-mesenchymal transition (EMT), in part through negative interactions with TGFβ1 induced Smad 2/3 activation. We utilized in vivo bleomycin-induced fibrosis models in the skin and lung to determine the potential therapeutic effect of BMP-7. We then determined the effect of BMP-7 on TGFβ1-induced EMT in lung epithelial cells and collagen production by human lung fibroblasts. We show that BMP-7 did not affect bleomycin-induced fibrosis in either the lung or skin in vivo; had no effect on expression of pro-fibrotic genes by human lung fibroblasts, either at rest or following exposure to TGFβ1; and did not modulate TGFβ1 -induced EMT in human lung epithelial cells. Taken together our data indicates that BMP-7 has no anti-fibrotic effect in lung or skin fibrosis either in vivo or in vitro. This suggests that the therapeutic options for BMP-7 may be confined to the renal compartment

Brain structural signatures of negative symptoms in depression and schizophrenia.

Negative symptoms occur in several major mental health disorders with undetermined mechanisms and unsatisfactory treatments; identification of their neural correlates might unveil the underlying pathophysiological basis and pinpoint the therapeutic targets. In this study, participants with major depressive disorder (n = 24), schizophrenia (n = 22), and healthy controls (n = 20) were assessed with 10 frequently used negative symptom scales followed by principal component analysis (PCA) of the scores. A linear model with the prominent components identified by PCA was then regressed on gray and white-matter volumes estimated from T1-weighted magnetic resonance imaging. In depressed patients, negative symptoms such as blunted affect, alogia, withdrawal, and cognitive impairment, assessed mostly via clinician-rated scales were inversely associated with gray matter volume in the bilateral cerebellum. In patients with schizophrenia, anhedonia, and avolition evaluated via self-rated scales inversely related to white-matter volume in the left anterior limb of internal capsule/anterior thalamic radiation and positively in the left superior longitudinal fasiculus. The pathophysiological mechanisms underlying negative symptoms might differ between depression and schizophrenia. These results also point to future negative symptom scale development primarily focused on detecting and monitoring the corresponding changes to brain structure or function.This work was supported by Brain and Behavior Research Foundation (NARSAD) and Medical Research Council (MRC) awards to GKM, and by the Wellcome Trust/MRC Behavioural and Clinical Neuroscience Institute, University of Cambridge. We thank Dr. Zheng Ye for her help with image analysis and technical support, Niels Reinders and staff at the Wolfson Brain Imaging Centre for help with data collection, and staff at IAPT, CAMEO and the Rehabilitation and Recovery Service in the Cambridgeshire and Peterborough NHS Foundation Trust for help with recruitment. The study was supported by infrastructure provided by the Wellcome Trust/MRC Behavioural and Clinical Neuroscience Institute at the University of Cambridge.This is the final version published by Frontiers here: http://journal.frontiersin.org/Journal/10.3389/fpsyt.2014.00116/abstract

Classification of Flat Directions in Perturbative Heterotic Superstring Vacua with Anomalous U(1)

We develop techniques to classify D- and F-flat directions for N=1 supersymmetric string vacua of the perturbative heterotic string theory, which possess an anomalous U(1) gauge group at the tree level. Genus-one corrections generate a Fayet-Iliopoulos term for the D-term of U(1)_A, which is canceled by non-zero vacuum expectation values (VEVs) of certain massless multiplets in such a way that the anomalous U(1) is broken, while maintaining the D- and F-flatness of the effective field theory. A systematic analysis of flat directions is given for non-zero VEVs of non-Abelian singlets, and the techniques are illustrated for a specific model. The approach sets the stage to classify the D- and F-flat directions for a large class of perturbative string vacua. This classification is a prerequisite to address systematically the phenomenological consequences of these models.Comment: 26 page

Reduction in ventral striatal activity when anticipating a reward in depression and schizophrenia: a replicated cross-diagnostic finding.

In the research domain framework (RDoC), dysfunctional reward expectation has been proposed to be a cross-diagnostic domain in psychiatry, which may contribute to symptoms common to various neuropsychiatric conditions, such as anhedonia or apathy/avolition. We used a modified version of the Monetary Incentive Delay (MID) paradigm to obtain functional MRI images from 22 patients with schizophrenia, 24 with depression and 21 controls. Anhedonia and other symptoms of depression, and overall positive and negative symptomatology were also measured. We hypothesized that the two clinical groups would have a reduced activity in the ventral striatum when anticipating reward (compared to anticipation of a neutral outcome) and that striatal activation would correlate with clinical measures of motivational problems and anhedonia. Results were consistent with the first hypothesis: two clusters in both the left and right ventral striatum were found to differ between the groups in reward anticipation. Post-hoc analysis showed that this was due to higher activation in the controls compared to the schizophrenia and the depression groups in the right ventral striatum, with activation differences between depression and controls also seen in the left ventral striatum. No differences were found between the two patient groups, and there were no areas of abnormal cortical activation in either group that survived correction for multiple comparisons. Reduced ventral striatal activity was related to greater anhedonia and overall depressive symptoms in the schizophrenia group, but not in the participants with depression. Findings are discussed in relation to previous literature but overall are supporting evidence of reward system dysfunction across the neuropsychiatric continuum, even if the specific clinical relevance is still not fully understood. We also discuss how the RDoC approach may help to solve some of the replication problems in psychiatric fMRI research.Supported by the Wellcome Trust Institutional Strategic Support Fund [097814/Z/11], a MRC Clinician Scientist [G0701911], a Brain and Behavior Research Foundation Young Investigator, and an Isaac Newton Trust award to Dr Murray; an award to Dr Segarra from the Secretary for Universities and Research of the Ministry of Economy and Knowledge of the Government of Catalonia and the European Union; by the University of Cambridge Behavioural and Clinical Neuroscience Institute, funded by a joint award from the Medical Research Council [G1000183]and Wellcome Trust [093875/Z/10/Z]; by awards from the Wellcome Trust [095692] and the Bernard Wolfe Health Neuroscience Fund to Dr. Fletcher, and by the Cambridge NIHR Biomedical Research Centre.This is the final version of the article. It first appeared from Frontiers via http://dx.doi.org/10.3389/fpsyg.2015.0128

Dicyclic Horizontal Symmetry and Supersymmetric Grand Unification

It is shown how to use as horizontal symmetry the dicyclic group $Q_6 \subset SU(2)$ in a supersymmetric unification $SU(5)\otimes SU(5)\otimes SU(2)$ where one $SU(5)$ acts on the first and second families, in a horizontal doublet, and the other acts on the third. This can lead to acceptable quark masses and mixings, with an economic choice of matter supermultiplets, and charged lepton masses can be accommodated.Comment: 10 pages, LaTe

Rational F-Theory GUTs without exotics

We construct F-theory GUT models without exotic matter, leading to the MSSM matter spectrum with potential singlet extensions. The interplay of engineering explicit geometric setups, absence of four-dimensional anomalies, and realistic phenomenology of the couplings places severe constraints on the allowed local models in a given geometry. In constructions based on the spectral cover we find no model satisfying all these requirements. We then provide a survey of models with additional U(1) symmetries arising from rational sections of the elliptic fibration in toric constructions and obtain phenomenologically appealing models based on SU(5) tops. Furthermore we perform a bottom-up exploration beyond the toric section constructions discussed in the literature so far and identify benchmark models passing all our criteria, which can serve as a guideline for future geometric engineering.Comment: 27 Pages, 1 Figur

Horizontal Symmetry for Quark and Squark Masses in Supersymmetric SU(5)

Recent interest in horizontal symmetry model building has been driven mainly by the large top mass and hence strong hierarchy in quark masses, and the possibility of appropriately constrained soft squark mass matrices, in place of an assumed universality condition, for satisfying the relevant FCNC constraints. Here we present the first successful SUSY-$SU(5)$ model that has such a feature. The horizontal symmetry is a gauged $(Q_{12} \times U(1))_H$ ($\subset (SU(2) \times U(1))_H$). All nonrenormalizable terms compatible with the symmetry are allowed in the mass matrix constructions. Charged lepton masses can also be accommodated.Comment: 15 pages, latex, 1 latex figure included version to be published in Phys. Rev. Lett. ; some small changes in notations and presentation, a small paragragh and 3 references adde

Amygdala and dlPFC abnormalities, with aberrant connectivity and habituation in response to emotional stimuli in females with BPD

Background: Little is known about the frontolimbic abnormalities thought to underlie borderline personality disorder (BPD). We endeavoured to study regional responses, as well as their connectivity and habituation during emotion processing. Methods: 14 BPD patients and 14 normal female controls (NC) controlled for menstrual phase underwent emotion-induction during an fMRI task using standardised images in a block design. We then performed psychophysiological interaction (PPI) analysis to investigate functional connectivity. Results: BPD patients reported more disgust in questionnaires compared to controls. Relative to NC, they showed reduced left amygdala and increased dorsolateral prefrontal cortex (dlPFC) activation to all emotions collapsed versus neutral. Habituation of ventral striatal activity to repeated emotional stimuli was observed in controls but not in BPD. Finally, in the context of disgust (but not other emotions) versus neutral, BPD patients displayed enhanced left amygdala coupling with the dlPFC and ventral striatum. Limitations: Strict inclusion criteria reduced the sample size. Conclusions: In summary, BPD showed abnormal patterns of activation, habituation and connectivity in regions linked to emotion regulation. Amygdala deactivation may be mediated by abnormal top-down regulatory control from the dorsolateral prefrontal cortex. Aberrant emotion processing may play a unique role in the pathophysiology of BPD