Near-infrared fluorescent imaging for parathyroid identification and/or preservation in surgery for primary hyperparathyroidism

Introduction: Near infrared autofluorescence (NIRAF) is a novel intraoperative technology that has shown promising results in the localisation of parathyroid glands (PGs) over the last decade. This study aimed to assess the potential utility of NIRAF in first time surgery for primary hyperparathyroidism (PHPT). Methods: An observational study over a period of 3 years in patients who underwent surgery for PHPT was designed. Data on the use of NIRAF and fluorescent patterns in different organs (thyroid and parathyroid) and parathyroid pathology (single versus multi-gland disease) were explored. In addition, cure rates and operating times were compared between the NIRAF and no-NIRAF groups to determine the potential value of NIRAF in this cohort. Results: In 230 patients undergoing first time surgery for PHPT, NIRAF was used in 50 patients. Of these 50 patients, NIRAF was considered to aid parathyroid identification in 9 patients (18%). The overall cure rate at 6 months of follow-up was 96.5% (98% in NIRAF and 96.1% without NIRAF; p=1.0). The median (interquartile range) operating time was longer in the NIRAF arm at 102 minutes (74-120 minutes) compared to the no-NIRAF arm at 75 minutes (75-109 minutes); however, this difference was not statistically significant (p=0.542). Although the median parathyroid to thyroid (P/T) auto-fluorescence (AF) ratio was similar between single gland and multi gland disease (2.5 vs to 2.76; p=1.0), the P/T AF ratio correlated negatively with increasing gland weight (p=0.038). Conclusion: The use of NIRAF resulted in some potential “surgeon-perceived” benefit but did not lead to improvements in cure rates. The negative correlation between fluorescent intensity and gland weight suggests loss of fluorescence with pathology, which needs further investigation. Further studies on larger cohorts of patients, in depth analysis of fluorescence patterns between normal, adenomatous, and hyperplastic glands and evaluation of user experience are needed. Primary hyperparathyroidism, hyperparathyroidism, autofluorescence, near-infrared fluorescence, parathyroid glands, endocrine, surgery

Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study

A41 Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study In: Addiction Science & Clinical Practice 2017, 12(Suppl 1): A4

Search for exclusive Higgs and Z boson decays to ϕγ and ργ with the ATLAS detector

A search for the exclusive decays of the Higgs and Z bosons to a φ or ρ meson and a photon is performed with a pp collision data sample corresponding to an integrated luminosity of up to 35.6 fb−1 collected at √s = 13 TeV with the ATLAS detector at the CERN Large Hadron Collider. These decays have been suggested as a probe of the Higgs boson couplings to light quarks. No significant excess of events is observed above the background, as expected from the Standard Model. Upper limits at 95% confidence level were obtained on the branching fractions of the Higgs boson decays to φγ and ργ of 4.8 × 10−4 and 8.8 × 10−4, respectively. The corresponding 95% confidence level upper limits for the Z boson decays are 0.9 × 10−6 and 25 × 10−6 for φγ and ργ, respectively

Search for long-lived neutral particles in pp collisions at s√=13 TeV that decay into displaced hadronic jets in the ATLAS calorimeter

This paper describes a search for pairs of neutral, long-lived particles decaying in the ATLAS calorimeter. Long-lived particles occur in many extensions to the Standard Model and may elude searches for new promptly decaying particles. The analysis considers neutral, long-lived scalars with masses between 5 and 400 GeV, produced from decays of heavy bosons with masses between 125 and 1000 GeV, where the long-lived scalars decay into Standard Model fermions. The analysis uses either 10.8 fb−1 or 33.0 fb−1 of data (depending on the trigger) recorded in 2016 at the LHC with the ATLAS detector in proton–proton collisions at a centre-of-mass energy of 13 TeV. No significant excess is observed, and limits are reported on the production cross section times branching ratio as a function of the proper decay length of the long-lived particles

Measurement of the top-quark mass using a leptonic invariant mass in pp collisions at s√ = 13 TeV with the ATLAS detector

A measurement of the top-quark mass (mt) in the tt¯ → lepton + jets channel is presented, with an experimental technique which exploits semileptonic decays of b-hadrons produced in the top-quark decay chain. The distribution of the invariant mass mℓμ of the lepton, ℓ (with ℓ = e, μ), from the W-boson decay and the muon, μ, originating from the b-hadron decay is reconstructed, and a binned-template profile likelihood fit is performed to extract mt. The measurement is based on data corresponding to an integrated luminosity of 36.1 fb−1 of s√ = 13 TeV pp collisions provided by the Large Hadron Collider and recorded by the ATLAS detector. The measured value of the top-quark mass is mt = 174.41 ± 0.39 (stat.) ± 0.66 (syst.) ± 0.25 (recoil) GeV, where the third uncertainty arises from changing the PYTHIA8 parton shower gluon-recoil scheme, used in top-quark decays, to a recently developed setup

Search for single vector-like B quark production and decay via B → bH(b¯b) in pp collisions at √s = 13 TeV with the ATLAS detector

A search is presented for single production of a vector-like B quark decaying into a Standard Model b-quark and a Standard Model Higgs boson, which decays into a b¯b pair. The search is carried out in 139 fb−1 of √s = 13 TeV proton-proton collision data collected by the ATLAS detector at the LHC between 2015 and 2018. No significant deviation from the Standard Model background prediction is observed, and mass-dependent exclusion limits at the 95% confidence level are set on the resonance production cross-section in several theoretical scenarios determined by the couplings cW, cZ and cH between the B quark and the Standard Model W, Z and Higgs bosons, respectively. For a vector-like B occurring as an isospin singlet, the search excludes values of cW greater than 0.45 for a B resonance mass (mB) between 1.0 and 1.2 TeV. For 1.2 TeV < mB < 2.0 TeV, cW values larger than 0.50–0.65 are excluded. If the B occurs as part of a (B, Y) doublet, the smallest excluded cZ coupling values range between 0.3 and 0.5 across the investigated resonance mass range 1.0 TeV < mB < 2.0 TeV

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease