Rare Top-quark Decays to Higgs boson in MSSM

In full one-loop generality and in next-to-leading order in QCD, we study rare top to Higgs boson flavour changing decay processes $t\to q h$ with $q=u,c$ quarks, in the general MSSM with R-parity conservation. Our primary goal is to search for enhanced effects on $Br(t\to q h)$ that could be visible at current and high luminosity LHC running. To this end, we perform an analytical expansion of the amplitude in terms of flavour changing squark mass insertions that treats both cases of hierarchical and degenerate squark masses in a unified way. We identify two enhanced effects allowed by various constraints: one from holomorphic trilinear soft SUSY breaking terms and/or right handed up squark mass insertions and another from non-holomorphic trilinear soft SUSY breaking terms and light Higgs boson masses. Interestingly, even with $\mathcal{O}(1)$ flavour violating effects in the, presently unconstrained, up-squark sector, SUSY effects on $Br(t\to q h)$ come out to be unobservable at LHC mainly due to leading order cancellations between penguin and self energy diagrams and the constraints from charge- and colour-breaking minima (CCB) of the MSSM vacuum. An exception to this conclusion may be effects arising from non-holomorphic soft SUSY breaking terms in the region where the CP-odd Higgs mass is smaller than the top-quark mass but this scenario is disfavoured by recent LHC searches. Our calculations for $t\to q h$ decay are made available in SUSY_FLAVOR numerical library.Comment: 32 pages, 6 figures; version accepted for publication in JHEP: additional comparison with literature added, minor misprints correcte

The decay h→γγh\to \gamma\gamma in the Standard-Model Effective Field Theory

Assuming that new physics effects are parametrized by the Standard-Model Effective Field Theory (SMEFT) written in a complete basis of up to dimension-6 operators, we calculate the CP-conserving one-loop amplitude for the decay $h\to \gamma\gamma$ in general $R_\xi$-gauges. We employ a simple renormalisation scheme that is hybrid between on-shell SM-like renormalised parameters and running $\overline{\mathrm{MS}}$ Wilson coefficients. The resulting amplitude is then finite, renormalisation scale invariant, independent of the gauge choice ($\xi$) and respects SM Ward identities. Remarkably, the $S$-matrix amplitude calculation resembles very closely the one usually known from renormalisable theories and can be automatised to a high degree. We use this gauge invariant amplitude and recent LHC data to check upon sensitivity to various Wilson coefficients entering from a more complete theory at the matching energy scale. We present a closed expression for the ratio $\mathcal{R}_{h\to \gamma\gamma}$, of the Beyond the SM versus the SM contributions as appeared in LHC $h\to \gamma\gamma$ searches. The most important contributions arise at tree level from the operators $Q_{\varphi B}, Q_{\varphi W}, Q_{\varphi WB}$, and at one-loop level from the dipole operators $Q_{uB},Q_{uW}$. Our calculation shows also that, for operators that appear at tree level in SMEFT, one-loop corrections can modify their contributions by less than 10%. Wilson coefficients corresponding to these five operators are bounded from current LHC $h\to \gamma\gamma$ data -- in some cases an order of magnitude stronger than from other searches. Finally, we correct results that appeared previously in the literature.Comment: 31 pages, 3 figures, v2: minor changes, one equation and references added; v3: subsection 5.3 removed and a paragraph added in Conclusions instead, references added, matches the published versio

Mass Insertions vs. Mass Eigenstates calculations in Flavour Physics

We present and prove a theorem of matrix analysis, the Flavour Expansion Theorem (or FET), according to which, an analytic function of a Hermitian matrix can be expanded polynomially in terms of its off-diagonal elements with coefficients being the divided differences of the analytic function and arguments the diagonal elements of the Hermitian matrix. The theorem is applicable in case of flavour changing amplitudes. At one-loop level this procedure is particularly natural due to the observation that every loop function in the Passarino-Veltman basis can be recursively expressed in terms of divided differences. FET helps to algebraically translate an amplitude written in mass eigenbasis into flavour mass insertions, without performing diagrammatic calculations in flavour basis. As a non-trivial application of FET up to a third order, we demonstrate its use in calculating strong bounds on the real parts of flavour changing mass insertions in the up- squark sector of the MSSM from neutron Electric Dipole Moment (nEDM) measurements, assuming that CP-violation arises only from the CKM matrix.Comment: 23 page

Editor's Choice - Delays to Surgery and Procedural Risks Following Carotid Endarterectomy in the UK National Vascular Registry.

OBJECTIVE: Guidelines recommend that patients suffering an ischaemic transient ischaemic attack (TIA) or stroke caused by carotid artery stenosis should undergo carotid endarterectomy (CEA) within 14 days. METHOD: The degree to which UK vascular units met this standard was examined and whether rapid interventions were associated with procedural risks. The study analysed patients undergoing CEA between January 2009 and December 2014 from 100 UK NHS hospitals. Data were collected on patient characteristics, intervals of time from symptoms to surgery, and 30-day postoperative outcomes. The relationship between outcomes and time from symptom to surgery was evaluated using multilevel multivariable logistic regression. RESULTS: In 23,235 patients, the median time from TIA/stroke to CEA decreased over time, from 22 days (IQR 10-56) in 2009 to 12 days (IQR 7-26) in 2014. The proportion of patients treated within 14 days increased from 37% to 58%. This improvement was produced by shorter times across the care pathway: symptoms to referral, from medical review to being seen by a vascular surgeon, and then to surgery. The spread of the median time from symptom to surgery among NHS hospitals shrank between 2009 and 2013 but then grew slightly. Low-, medium-, and high-volume NHS hospitals all improved their performance similarly. Performing CEA within 48 h of symptom onset was associated with a small increase in the 30-day stroke and death rate: 3.1% (0-2 days) compared with 2.0% (3-7 days); adjusted odds ratio 1.64 (95% CI 1.04-2.59) but not with longer delays. CONCLUSIONS: The delay from symptom to CEA in symptomatic patients with ipsilateral 50-99% carotid stenoses has reduced substantially, although 42% of patients underwent CEA after the recommended 14 days. The risk of stroke after CEA was low, but there may be a small increase in risk during the first 48 h after symptoms

Hartley transform and the use of the Whitened Hartley spectrum as a tool for phase spectral processing

The Hartley transform is a mathematical transformation which is closely related to the better known Fourier transform. The properties that differentiate the Hartley Transform from its Fourier counterpart are that the forward and the inverse transforms are identical and also that the Hartley transform of a real signal is a real function of frequency. The Whitened Hartley spectrum, which stems from the Hartley transform, is a bounded function that encapsulates the phase content of a signal. The Whitened Hartley spectrum, unlike the Fourier phase spectrum, is a function that does not suffer from discontinuities or wrapping ambiguities. An overview on how the Whitened Hartley spectrum encapsulates the phase content of a signal more efficiently compared with its Fourier counterpart as well as the reason that phase unwrapping is not necessary for the Whitened Hartley spectrum, are provided in this study. Moreover, in this study, the product–convolution relationship, the time-shift property and the power spectral density function of the Hartley transform are presented. Finally, a short-time analysis of the Whitened Hartley spectrum as well as the considerations related to the estimation of the phase spectral content of a signal via the Hartley transform, are elaborated

Incident venous thromboembolic events in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER)

<p>Background: Venous thromboembolic events (VTE), including deep venous thrombosis and pulmonary embolism, are common in older age. It has been suggested that statins might reduce the risk of VTE however positive results from studies of middle aged subjects may not be generalisable to elderly people. We aimed to determine the effect of pravastatin on incident VTE in older people; we also studied the impact of clinical and plasma risk variables.</p> <p>Methods: This study was an analysis of incident VTE using data from the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER), a randomized, double-blind, placebo-controlled trial of pravastatin in men and women aged 70-82. Mean follow-up was 3.2 years. Risk for VTE was examined in non-warfarin treated pravastatin (n = 2834) and placebo (n = 2865) patients using a Cox's proportional hazard model, and the impact of other risk factors assessed in a multivariate forward stepwise regression analysis. Baseline clinical characteristics, blood biochemistry and hematology variables, plasma levels of lipids and lipoproteins, and plasma markers of inflammation and adiposity were compared. Plasma markers of thrombosis and hemostasis were assessed in a nested case (n = 48) control (n = 93) study where the cohort was those participants, not on warfarin, for whom data were available.</p> <p>Results: There were 28 definite cases (1.0%) of incident VTE in the pravastatin group recipients and 20 cases (0.70%) in placebo recipients. Pravastatin did not reduce VTE in PROSPER compared to placebo [unadjusted hazard ratio (95% confidence interval) 1.42 (0.80, 2.52) p = 0.23]. Higher body mass index (BMI) [1.09 (1.02, 1.15) p = 0.0075], country [Scotland vs Netherlands 4.26 (1.00, 18.21) p = 0.050 and Ireland vs Netherlands 6.16 (1.46, 26.00) p = 0.013], lower systolic blood pressure [1.35 (1.03, 1.75) p = 0.027] and lower baseline Mini Mental State Examination (MMSE) score [1.19 (1.01, 1.41) p = 0.034] were associated with an increased risk of VTE, however only BMI, country and systolic blood pressure remained significant on multivariate analysis. In a nested case control study of definite VTE, plasma Factor VIII levels were associated with VTE [1.52 (1.01, 2.28), p = 0.044]. However no other measure of thrombosis and haemostasis was associated with increased risk of VTE.</p> <p>Conclusions: Pravastatin does not prevent VTE in elderly people at risk of vascular disease. Blood markers of haemostasis and inflammation are not strongly predictive of VTE in older age however BMI, country and lower systolic blood pressure are independently associated with VTE risk.</p&gt

Simvastatin inhibits TLR8 signaling in primary human monocytes and spontaneous TNF production from rheumatoid synovial membrane cultures

Simvastatin has been shown to have anti-inflammatory effects that are independent of its serum cholesterol lowering action, but the mechanisms by which these anti-inflammatory effects are mediated have not been elucidated. To explore the mechanism involved, the effect of simvastatin on Toll-like receptor (TLR) signalling in primary human monocytes was investigated. A short pre-treatment with simvastatin dose-dependently inhibited the production of tumor necrosis factor-α (TNF) in response to TLR8 (but not TLRs 2, 4, or 5) activation. Statins are known inhibitors of the cholesterol biosynthetic pathway, but intriguingly TLR8 inhibition could not be reversed by addition of mevalonate or geranylgeranyl pyrophosphate; downstream products of cholesterol biosynthesis. TLR8 signalling was examined in HEK 293 cells stably expressing TLR8, where simvastatin inhibited IKKα/β phosphorylation and subsequent NF-κB activation without affecting the pathway to AP-1. Since simvastatin has been reported to have anti-inflammatory effects in RA patients and TLR8 signalling contributes to TNF production in human RA synovial tissue in culture, simvastatin was tested in these cultures. Simvastatin significantly inhibited the spontaneous release of TNF in this model which was not reversed by mevalonate. Together, these results demonstrate a hitherto unrecognized mechanism of simvastatin inhibition of TLR8 signalling that may in part explain its beneficial anti-inflammatory effects