Measurement of associated Z plus charm production in proton-proton collisions at root s=8TeV

A study of the associated production of a Z boson and a charm quark jet (Z + c), and a comparison to production with a b quark jet (Z + b), in pp collisions at a centre-of-mass energy of 8 TeV are presented. The analysis uses a data sample corresponding to an integrated luminosity of 19.7 fb(-1), collected with the CMS detector at the CERN LHC. The Z boson candidates are identified through their decays into pairs of electrons or muons. Jets originating from heavy flavour quarks are identified using semileptonic decays of c or b flavoured hadrons and hadronic decays of charm hadrons. The measurements are performed in the kinematic region with two leptons with pT(l) > 20 GeV, vertical bar eta(l)vertical bar 25 GeV and vertical bar eta(jet)vertical bar Z + c + X) B(Z -> l(+)l(-)) = 8.8 +/- 0.5 (stat)+/- 0.6 (syst) pb. The ratio of the Z+c and Z+b production cross sections is measured to be sigma(pp -> Z+c+X)/sigma (pp -> Z+b+X) = 2.0 +/- 0.2 (stat)+/- 0.2 (syst). The Z+c production cross section and the cross section ratio are also measured as a function of the transverse momentum of theZ boson and of the heavy flavour jet. The measurements are compared with theoretical predictions.Peer reviewe

Measurement of the underlying event activity in inclusive Z boson production in proton-proton collisions at root s=13 TeV

This paper presents a measurement of the underlying event activity in proton-proton collisions at a center-of-mass energy of 13TeV, performed using inclusive Z boson production events collected with the CMS experiment at the LHC. The analyzed data correspond to an integrated luminosity of 2.1 fb(-1). The underlying event activity is quantified in terms of the charged particle multiplicity, as well as of the scalar sum of the charged particles' transverse momenta in different topological regions defined with respect to the Z boson direction. The distributions are unfolded to the stable particle level and compared with predictions from various Monte Carlo event generators, as well as with similar CDF and CMS measurements at center-of-mass energies of 1.96 and 7TeV respectively.Peer reviewe

Updates in SJS/TEN: collaboration, innovation, and community

Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN) is a predominantly drug-induced disease, with a mortality rate of 15–20%, that engages the expertise of multiple disciplines: dermatology, allergy, immunology, clinical pharmacology, burn surgery, ophthalmology, urogynecology, and psychiatry. SJS/TEN has an incidence of 1–5/million persons per year in the United States, with even higher rates globally. One of the challenges of SJS/TEN has been developing the research infrastructure and coordination to answer questions capable of transforming clinical care and leading to improved patient outcomes. SJS/TEN 2021, the third research meeting of its kind, was held as a virtual meeting on August 28–29, 2021. The meeting brought together 428 international scientists, in addition to a community of 140 SJS/TEN survivors and family members. The goal of the meeting was to brainstorm strategies to support the continued growth of an international SJS/TEN research network, bridging science and the community. The community workshop section of the meeting focused on eight primary themes: mental health, eye care, SJS/TEN in children, non-drug induced SJS/TEN, long-term health complications, new advances in mechanisms and basic science, managing long-term scarring, considerations for skin of color, and COVID-19 vaccines. The meeting featured several important updates and identified areas of unmet research and clinical need that will be highlighted in this white paper

Glutathione Dysregulation, Cardiac Oxidative Stress, and Inflammation during n-6 Polyunsaturated Fatty Acid Overload

Historically dietary saturated fats were blamed for cardiovascular disease (CVD). However, lowering dietary saturated fats did not curb CVD rates and instead detrimental roles of n-6 polyunsaturated fatty acid (n-6 PUFA) which was used to substitute saturated fats have come to the forefront. My objective was to identify mechanisms leading to dietary n-6 PUFA induced CVDs using mice and cell models. Here isocaloric diets rich in n-6 PUFA or monounsaturated fatty acids (MUFA) were used in vivo or cardiac cells like cardiomyocytes and fibroblasts were incubated with n-6 PUFA or MUFA in vitro. We established that n-6 PUFA reduced glutathione (GSH), promoted oxidative stress and impaired mitochondrial function. n-6 PUFA diets also increased pro-inflammatory cytokines and impaired GSH synthesis in vivo. Removal of a primary pro-inflammatory stimulus by using mice deficient in monocyte chemotactic protein 1 (MCP-1) restored GSH and lowered inflammation in n-6 PUFA-fed MCP-1-/- mice (chapter 2). Although inflammatory biomarkers were high in n-6 PUFA incubated cells, treatment with LPS lowered murine macrophage function suggesting a dysregulated immune response. This dysregulated immune response was also reversed by increasing GSH in macrophages. These data indicate that n-6 PUFA increases inflammatory biomarkers but impairs macrophage function due to GSH depletion (chapter 3). Finally, as cell death is a major contributor to CVD, my final chapter 4 showed that under cardiac stress induced by beta-adrenergic agonist, isoproterenol, n-6 PUFA promotes necrosis, increases in cytochrome P450-induced metabolites and a reduction in DNA repair genes. Overall, these results show the key roles of GSH dysregulation in n-6 PUFA induced inflammation, which could be key novel mediator of PUFA-specific cardiotoxicity in the Western world.Arts and Sciences, Irving K. Barber School of (Okanagan)Biology, Department of (Okanagan)Graduat

Analysis using national databases reveals a positive association between dietary polyunsaturated fatty acids with TV watching and diabetes in European females - Fig 2

<p>Partial regression plot (a) showing the association between sedentary behaviour of 11 year old girls and mean PUFA, holding all other predictors in the multiple regression constant (N = 21; <i>P</i>< 0.001). Grey shading indicates confidence bands around the regression line (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0173084#pone.0173084.t004" target="_blank">Table 4A</a> for details). Shown in panel (b) is the least-squares regression betweensedentary behaviour of 11 year old girls and mean PUFA, without any other predictors. The regression is highly significant (N = 21; R²_adj = 0.50; <i>P</i> = 0.002).</p

Regulatory Connections between Iron and Glucose Metabolism

Iron is essential for energy metabolism, and states of iron deficiency or excess are detrimental for organisms and cells. Therefore, iron and carbohydrate metabolism are tightly regulated. Serum iron and glucose levels are subjected to hormonal regulation by hepcidin and insulin, respectively. Hepcidin is a liver-derived peptide hormone that inactivates the iron exporter ferroportin in target cells, thereby limiting iron efflux to the bloodstream. Insulin is a protein hormone secreted from pancreatic &beta;-cells that stimulates glucose uptake and metabolism via insulin receptor signaling. There is increasing evidence that systemic, but also cellular iron and glucose metabolic pathways are interconnected. This review article presents relevant data derived primarily from mouse models and biochemical studies. In addition, it discusses iron and glucose metabolism in the context of human disease