Combined Explanation of the Z→bb[over ¯] Forward-Backward Asymmetry, the Cabibbo Angle Anomaly, and τ→µνν and b→sℓ

In this Letter, we propose a simple model that can provide a combined explanation of the Z→bb[over ¯] forward-backward asymmetry, the Cabibbo angle anomaly (CAA), τ→µνν and b→sℓ^{+}ℓ^{-} data. This model is obtained by extending the standard model (SM) by two heavy vectorlike quarks (an SU(2)_{L} doublet (singlet) with hypercharge -5/6 (-1/3), two new scalars (a neutral and a singly charged one), and a gauged L_{µ}-L_{τ} symmetry. The mixing of the new quarks with the SM ones, after electroweak symmetry breaking, does not only explain Z→bb[over ¯] data, but also generates a lepton flavor universal contribution to b→sℓ^{+}ℓ^{-} transitions. Together with the lepton flavor universality violating effect, generated by loop-induced Z^{'} penguins involving the charged scalar and the heavy quarks, it gives an excellent fit to data (6.1σ better than the SM). Furthermore, the charged scalar (neutral vector) gives a necessarily constructive tree-level (loop) effect in µâ†’eνν (τ→µνν), which can naturally account for the CAA (Br[τ→µνν]/Br[τ→eνν] and Br[τ→µνν]/Br[µâ†’eνν]).

Calcitonin Screening in Nodular Thyroid Disease: Is There a Definitive Answer?

INTRODUCTION: Calcitonin (Ctn) is a hormone secreted by thyroid "C" cells and is considered an excellent marker for medullary thyroid carcinoma (MTC). However, the use of Ctn to screen patients with nodular thyroid disease (NTD) remains controversial. OBJECTIVE: The aim of this work was to define the frequency of hypercalcitoninemia among NTD patients followed at a tertiary referral hospital. METHODS: A retrospective analysis was made of basal Ctn measurements and corresponding patients' records between January 2011 and December 2015. Hypercalcitoninemia was defined as > 10 pg/mL. Depending on the Ctn value, three groups were considered: G1, ≤10 pg/mL; G2, 10-100 pg/mL; G3, ≥100 pg/mL. RESULTS: Ctn was requested in an NTD context for 1,504 patients, 69 of whom had hypercalcitoninemia. Of these, 20 underwent surgery (G2, 11; G3, 9), and a histological diagnosis of MTC was established in 12 (G2, 3/27%; G3, 9/100%). Surgery was chosen based solely on Ctn levels in 7 cases, since only 5 had a positive cytology. CONCLUSIONS: Hypercalcitoninemia was found in 4.6% of NTD patients. Ctn levels ≥100 pg/mL were associated with a greater CMT risk than values between 10 and 100 pg/mL, reinforcing results from other groups. The need for an adequate interpretation of results as well as an appropriate selection of patients to surgery stresses the importance of endocrinologists requesting and interpreting results.

Searching for New Physics with b→sτ

In recent years, intriguing hints for the violation of lepton flavor universality (LFU) have been accumulated in semileptonic B decays, both in the charged-current transitions b→cℓ^{-}ν[over ¯]_{ℓ} (i.e., R_{D}, R_{D^{*}}, and R_{J/ψ}) and the neutral-current transitions b→sℓ^{+}ℓ^{-} (i.e., R_{K} and R_{K^{*}}). Hints for LFU violation in R_{D^{(*)}} and R_{J/ψ} point at large deviations from the standard model (SM) in processes involving tau leptons. Moreover, LHCb has reported deviations from the SM expectations in b→sµ^{+}µ^{-} processes as well as in the ratios R_{K} and R_{K^{*}}, which together point at new physics (NP) affecting muons with a high significance. These hints for NP suggest the possibility of huge LFU-violating effects in b→sτ^{+}τ^{-} transitions. In this Letter, we predict the branching ratios of B→Kτ^{+}τ^{-}, B→K^{*}τ^{+}τ^{-}, and B_{s}→ϕτ^{+}τ^{-}, taking into account NP effects in the Wilson coefficients C_{9(^{'})}^{ττ} and C_{10(^{'})}^{ττ}. Assuming a common NP explanation of R_{D}, R_{D^{(*)}}, and R_{J/ψ}, we show that a very large enhancement of b→sτ^{+}τ^{-} processes, of around 3 orders of magnitude compared to the SM, can be expected under fairly general assumptions. We find that the branching ratios of B_{s}→τ^{+}τ^{-}, B_{s}→ϕτ^{+}τ^{-}, and B→K^{(*)}τ^{+}τ^{-} under these assumptions are in the observable range for LHCb and Belle II.

Influence of body mass index in anti-Müllerian hormone levels in 951 non-polycystic ovarian syndrome women followed at a reproductive medicine unit.

PURPOSE: Anti-Müllerian hormone (AMH) is a useful marker of ovarian reserve. Obesity/overweight are increasing and may affect the reproductive health. Previous studies regarding the effect of body mass index (BMI) on AMH levels are discordant. Our main goal was to evaluate the influence of BMI on AMH levels in women without polycystic ovarian syndrome. METHODS: Revision of medical records of 951 women who performed AMH determinations as part of their fertility workup, between 2011 and 2016. RESULTS: Median AMH concentration was 1.75 [interquartile range (IQR) 2] ng/mL (12.9 pmol/mL) and median age at AMH determination was 35 (IQR 6) years. These women evidenced a median BMI of 23 (IQR 5) kg/m2. Caucasian women were more represented [889(89.3%)]. Smoking habits (present/past) were present in 359(36.1%), and 147(14.8%) harboured a history of ovarian surgery. On univariable analysis AMH was not correlated with BMI (r = 0.048/p = 0.135); the only factors influencing AMH were age (p < 0.001), ethnicity (p = 0.004), and previous ovarian surgery (p < 0.001). On multivariable analysis, age was the only variable significantly associated with AMH, evidencing a reduction of 6.2% for each additional year (p < 0.0001). Furthermore, we verified a trend suggesting an AMH reduction of 22% (p = 0.08) in black patients comparing with the caucasian ones, when controlling for the other variables. CONCLUSION: We report one of the largest series evaluating the influence of BMI on AMH levels and, consequently, on ovarian reserve. BMI does not seem to affect AMH levels. The reported concerns on infertility in overweight and obese women may be related to follicular development/oocyte maturation or endometrial disorders, rather than decreased ovarian reserve.

N-terminal probrain natriuretic peptide as a biomarker of cardioembolic stroke.

BACKGROUND: and purpose N-terminal probrain natriuretic peptide, which is mainly produced by the heart, is increased in acute stroke. We aimed to determine if N-terminal probrain natriuretic peptide could be a biomarker for ischemic stroke with a cardioembolic cause. METHODS: Consecutive sample of acute stroke patients admitted to a Stroke Unit. Ischemic stroke subtype was classified using the TOAST classification. Blood samples were drawn within 72 h after stroke onset. Serum N-terminal probrain natriuretic peptide concentration was measured using an electrochemiluminescence immunoassay. Mean values of N-terminal probrain natriuretic peptide were compared between patients with hemorrhagic stroke vs. ischemic stroke, cardioembolic stroke vs. noncardioembolic stroke, cardioembolic stroke with atrial fibrillation vs. noncardioembolic stroke using t-test. Receiver operating characteristic curves were used to test the ability of N-terminal probrain natriuretic peptide values to identify cardioembolic stroke and cardioembolic stroke with atrial fibrillation. RESULTS: Ninety-two patients were included (66 with ischemic stroke) with a mean age of 58·6 years. Twenty-eight (42·4%) ischemic strokes had a cardioembolic cause. Mean N-terminal probrain natriuretic peptide values for cardioembolic stroke were significantly higher (P<0·001) (491·6; 95% confidence interval 283·7-852·0 pg/ml) than for noncardioembolic ischemic stroke (124·7; 86·3-180·2 pg/ml). The area under the receiver operating characteristic curve for N-terminal probrain natriuretic peptide in cardioembolic stroke was 0·77. The cut-off point with the highest sensitivity and specificity was set at 265·5 pg/ml (71·4% and 73·7% respectively). The area under the curve of N-terminal probrain natriuretic peptide for cardioembolic stroke related to atrial fibrillation was 0·92, cut-off was set at 265·5 pg/ml (sensitivity 94·4%, specificity 72·9%). CONCLUSION: N-terminal probrain natriuretic peptide is a biomarker with a good accuracy to predict ischemic stroke of cardioembolic cause, namely associated with atrial fibrillation.

Exploring Bd,s-->KK decays through flavor symmetries and QCD factorization.

We present a new analysis of Bd,s-->KK modes within the standard model (SM), relating them in a controlled way through SU(3)-flavor symmetry and QCD-improved factorization. We propose a set of sum rules for Bd,s-->K0K0 observables. We determine Bs-->KK branching ratios and CP asymmetries as functions of Adir(Bd-->K0K0), pointing out a conflict between BR(Bs-->K+K-) in the SM and data. Finally, we predict the amount of U-spin breaking between Bd-->pi+pi- and Bs-->K+K-.