1,920 research outputs found
A Geometric Approach to CP Violation: Applications to the MCPMFV SUSY Model
We analyze the constraints imposed by experimental upper limits on electric
dipole moments (EDMs) within the Maximally CP- and Minimally Flavour-Violating
(MCPMFV) version of the MSSM. Since the MCPMFV scenario has 6 non-standard
CP-violating phases, in addition to the CP-odd QCD vacuum phase \theta_QCD,
cancellations may occur among the CP-violating contributions to the three
measured EDMs, those of the Thallium, neutron and Mercury, leaving open the
possibility of relatively large values of the other CP-violating observables.
We develop a novel geometric method that uses the small-phase approximation as
a starting point, takes the existing EDM constraints into account, and enables
us to find maximal values of other CP-violating observables, such as the EDMs
of the Deuteron and muon, the CP-violating asymmetry in b --> s \gamma decay,
and the B_s mixing phase. We apply this geometric method to provide upper
limits on these observables within specific benchmark supersymmetric scenarios,
including extensions that allow for a non-zero \theta_QCD.Comment: 34 pages, 16 eps figures, to appear in JHE
Gauge-theoretic invariants for topological insulators: A bridge between Berry, Wess-Zumino, and Fu-Kane-Mele
We establish a connection between two recently-proposed approaches to the
understanding of the geometric origin of the Fu-Kane-Mele invariant
, arising in the context of 2-dimensional
time-reversal symmetric topological insulators. On the one hand, the
invariant can be formulated in terms of the Berry connection and
the Berry curvature of the Bloch bundle of occupied states over the Brillouin
torus. On the other, using techniques from the theory of bundle gerbes it is
possible to provide an expression for containing the square root
of the Wess-Zumino amplitude for a certain -valued field over the
Brillouin torus.
We link the two formulas by showing directly the equality between the above
mentioned Wess-Zumino amplitude and the Berry phase, as well as between their
square roots. An essential tool of independent interest is an equivariant
version of the adjoint Polyakov-Wiegmann formula for fields , of which we provide a proof employing only basic homotopy theory and
circumventing the language of bundle gerbes.Comment: 23 pages, 1 figure. To appear in Letters in Mathematical Physic
A Comprehensive Analysis of Electric Dipole Moment Constraints on CP-violating Phases in the MSSM
We analyze the constraints placed on individual, flavor diagonal CP-violating
phases in the minimal supersymmetric extension of the Standard Model (MSSM) by
current experimental bounds on the electric dipole moments (EDMs) of the
neutron, Thallium, and Mercury atoms. We identify the four CP-violating phases
that are individually highly constrained by current EDM bounds, and we explore
how these phases and correlations among them are constrained by current EDM
limits. We also analyze the prospective implications of the next generation of
EDM experiments. We point out that all other CP-violating phases in the MSSM
are not nearly as tightly constrained by limits on the size of EDMs. We
emphasize that a rich set of phenomenological consequences is potentially
associated with these generically large EDM-allowed phases, ranging from B
physics, electroweak baryogenesis, and signals of CP-violation at the CERN
Large Hadron Collider and at future linear colliders. Our numerical study takes
into account the complete set of contributions from one- and two-loop EDMs of
the electron and quarks, one- and two-loop Chromo-EDMs of quarks, the Weinberg
3-gluon operator, and dominant 4-fermion CP-odd operator contributions,
including contributions which are both included and not included yet in the
CPsuperH2.0 package. We also introduce an open-source numerical package, 2LEDM,
which provides the complete set of two-loop electroweak diagrams contributing
to the electric dipole moments of leptons and quarks.Comment: 23 pages, 11 figures; v2: references added, minor change
Structure of hadron resonances with a nearby zero of the amplitude
We discuss the relation between the analytic structure of the scattering
amplitude and the origin of an eigenstate represented by a pole of the
amplitude.If the eigenstate is not dynamically generated by the interaction in
the channel of interest, the residue of the pole vanishes in the zero coupling
limit. Based on the topological nature of the phase of the scattering
amplitude, we show that the pole must encounter with the
Castillejo-Dalitz-Dyson (CDD) zero in this limit. It is concluded that the
dynamical component of the eigenstate is small if a CDD zero exists near the
eigenstate pole. We show that the line shape of the resonance is distorted from
the Breit-Wigner form as an observable consequence of the nearby CDD zero.
Finally, studying the positions of poles and CDD zeros of the KbarN-piSigma
amplitude, we discuss the origin of the eigenstates in the Lambda(1405) region.Comment: 7 pages, 3 figures, v2: published versio
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Improved Constraints on Sterile Neutrino Mixing from Disappearance Searches in the MINOS, MINOS+, Daya Bay, and Bugey-3 Experiments.
Searches for electron antineutrino, muon neutrino, and muon antineutrino disappearance driven by sterile neutrino mixing have been carried out by the Daya Bay and MINOS+ collaborations. This Letter presents the combined results of these searches, along with exclusion results from the Bugey-3 reactor experiment, framed in a minimally extended four-neutrino scenario. Significantly improved constraints on the θ_{Îźe} mixing angle are derived that constitute the most constraining limits to date over five orders of magnitude in the mass-squared splitting Îm_{41}^{2}, excluding the 90% C.L. sterile-neutrino parameter space allowed by the LSND and MiniBooNE observations at 90% CL_{s} for Îm_{41}^{2}<13ââeV^{2}. Furthermore, the LSND and MiniBooNE 99% C.L. allowed regions are excluded at 99% CL_{s} for Îm_{41}^{2}<1.6âeV^{2}
The Surgical Infection Society revised guidelines on the management of intra-abdominal infection
Background: Previous evidence-based guidelines on the management of intra-abdominal infection (IAI) were published by the Surgical Infection Society (SIS) in 1992, 2002, and 2010. At the time the most recent guideline was released, the plan was to update the guideline every five years to ensure the timeliness and appropriateness of the recommendations.
Methods: Based on the previous guidelines, the task force outlined a number of topics related to the treatment of patients with IAI and then developed key questions on these various topics. All questions were approached using general and specific literature searches, focusing on articles and other information published since 2008. These publications and additional materials published before 2008 were reviewed by the task force as a whole or by individual subgroups as to relevance to individual questions. Recommendations were developed by a process of iterative consensus, with all task force members voting to accept or reject each recommendation. Grading was based on the GRADE (Grades of Recommendation Assessment, Development, and Evaluation) system; the quality of the evidence was graded as high, moderate, or weak, and the strength of the recommendation was graded as strong or weak. Review of the document was performed by members of the SIS who were not on the task force. After responses were made to all critiques, the document was approved as an official guideline of the SIS by the Executive Council.
Results: This guideline summarizes the current recommendations developed by the task force on the treatment of patients who have IAI. Evidence-based recommendations have been made regarding risk assessment in individual patients; source control; the timing, selection, and duration of antimicrobial therapy; and suggested approaches to patients who fail initial therapy. Additional recommendations related to the treatment of pediatric patients with IAI have been included.
Summary: The current recommendations of the SIS regarding the treatment of patients with IAI are provided in this guideline
Hsa-miR-125a-3p and hsa-miR-125a-5p are downregulated in non-small cell lung cancer and have inverse effects on invasion and migration of lung cancer cells
<p>Abstract</p> <p>Background</p> <p>Two mature microRNAs (miRNAs), hsa-miR-125a-3p and hsa-miR-125a-5p (collectively referred to as hsa-miR-125a-3p/5p), are derived from 3' and 5' ends of pre-miR-125a, respectively. Although impaired regulation of hsa-miR-125a-5p has been observed in some tumors, the role of this miRNA in invasion and metastasis remains unclear, and few studies have examined the function of hsa-miR-125a-3p. In order to characterize the functions of hsa-miR-125a-3p/5p in invasion and metastasis of non-small cell lung cancer (NSCLC), we investigated the relationships between hsa-miR-125a-3p/5p expression and lymph node metastasis in NSCLC tissues. We also explored the impact of expression of these miRNAs on invasive and migratory capabilities of lung cancer cells.</p> <p>Methods</p> <p>Expression of hsa-miR-125a-3p/5p in NSCLC tissues was explored using real-time PCR. The relationships between hsa-miR-125a-3p/5p expression and pathological stage or lymph node metastasis were assessed using the Spearman correlation test. For in vitro studies, lung cancer cells were transfected with sense and antisense 2'-O-methyl oligonucleotides for gain-of-function and loss-of-function experiments. Transwell experiments were performed to evaluate cellular migration and invasion.</p> <p>Results</p> <p>Expression of hsa-miR-125a-3p/5p was lower in NSCLC tissues than in adjacent normal lung tissues (LAC). Furthermore, the results from the Spearman correlation test showed a negative relationship between hsa-miR-125a-3p expression and pathological stage or lymph node metastasis and an inverse relationship between hsa-miR-125a-5p expression and pathological stage or lymph node metastasis. In vitro gain-of-function experiments indicated that hsa-miR-125a-3p and hsa-miR-125a-5p function in an opposing manner, suppressing or enhancing cell migration and invasion in A549 and SPC-A-1 cell lines, respectively. These opposing functions were further validated by suppression of hsa-miR-125a-3p and hsa-miR-125a-5p expression in loss-of-function experiments.</p> <p>Conclusion</p> <p>Hsa-miR-125a-3p and hsa-miR-125a-5p play distinct roles in regulation of invasive and metastatic capabilities of lung cancer cells, consistent with the opposing correlations between the expression of these miRNAs and lymph node metastasis in NSCLC. These results provide new insights into the roles of miR-125a family members in the development of NSCLC.</p
Actomyosin and vimentin cytoskeletal networks regulate nuclear shape, mechanics and chromatin organization
This work was supported in part by a Marie Curie CIG grant (PCIG14-GA-2013-631011 CSKFingerprints) and a BBSRC grant (BB/P006108/1). MCK is supported by a PhD studentship from the Life Sciences Initiative at QMUL
A novel hypoxia-dependent 2-nitroimidazole KIN-841 inhibits tumour-specific angiogenesis by blocking production of angiogenic factors
Autism as a disorder of neural information processing: directions for research and targets for therapy
The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which theyfeed, is hampered bythe large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself
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