Oral cancer awareness of undergraduate medical and dental students

<p>Abstract</p> <p>Background</p> <p>The incidence of oral cancer is increasing in the United Kingdom. Early detection of oral cancers makes them more amenable to treatment and allows the greatest chance of cure. Delay in presentation and/or referral has a significant effect on the associated morbidity and mortality. Lack of general medical practitioner and general dental practitioner oral cancer knowledge has been shown to contribute to delays in referral and treatment. The aim of this study was to investigate the oral cancer awareness of future general medical and general dental practitioners by assessing undergraduate medical and dental students' knowledge of prevention and early detection of oral cancer.</p> <p>Method</p> <p>Questionnaires were delivered to undergraduate medical and dental students at the University of Dundee, assessing oral examination habits, delivery of advice on oral cancer risk factors, knowledge of oral cancer risk factors and clinical appearance, preferred point of referral and requests for further information.</p> <p>Results</p> <p>Undergraduate medical students were less likely to examine patients' oral mucosa routinely and less likely to advise patients about risk factors for oral cancer. Medical students identified fewer oral cancer risk factors. In particular alcohol use was identified poorly. Medical students also identified fewer oral changes associated with oral cancer. Erythroplakia and erythroleukoplakia were identified poorly. Medical students felt less well informed regarding oral cancer. 86% and 92% of undergraduate medical and dental students respectively requested further information about oral cancer.</p> <p>Conclusion</p> <p>This study highlights the need for improved education of undergraduate medical and dental students regarding oral cancer.</p

Gene polymorphisms against DNA damage induced by hydrogen peroxide in leukocytes of healthy humans through comet assay: a quasi-experimental study

<p>Abstract</p> <p>Background</p> <p>Normal cellular metabolism is well established as the source of endogenous reactive oxygen species which account for the background levels of oxidative DNA damage detected in normal tissue. Hydrogen peroxide imposes an oxidative stress condition on cells that can result in DNA damage, leading to mutagenesis and cell death. Several potentially significant genetic variants related to oxidative stress have already been identified, and angiotensin I-converting enzyme (ACE) inhibitors have been reported as possible antioxidant agents that can reduce vascular oxidative stress in cardiovascular events.</p> <p>Methods</p> <p>We investigate the influences of haptoglobin, manganese superoxide dismutase (MnSOD Val9Ala), catalase (CAT -21A/T), glutathione peroxidase 1 (GPx-1 Pro198Leu), ACE (I/D) and gluthatione S-transferases GSTM1 and GSTT1 gene polymorphisms against DNA damage and oxidative stress. These were induced by exposing leukocytes from peripheral blood of healthy humans (N = 135) to hydrogen peroxide (H₂O₂), and the effects were tested by comet assay. Blood samples were submitted to genotyping and comet assay (before and after treatment with H₂O₂at 250 μM and 1 mM).</p> <p>Results</p> <p>After treatment with H₂O₂at 250 μM, the GPx-1 polymorphism significantly influenced results of comet assay and a possible association of the Pro/Leu genotype with higher DNA damage was found. The highest or lowest DNA damage also depended on interaction between GPX-1/ACE and Hp/GSTM1T1 polymorphisms when hydrogen peroxide treatment increased oxidative stress.</p> <p>Conclusions</p> <p>The GPx-1 polymorphism and the interactions between GPX-1/ACE and Hp/GSTM1T1 can be determining factors for DNA oxidation provoked by hydrogen peroxide, and thus for higher susceptibility to or protection against oxidative stress suffered by healthy individuals.</p

Search for pair-produced long-lived neutral particles decaying to jets in the ATLAS hadronic calorimeter in ppcollisions at √s=8TeV

The ATLAS detector at the Large Hadron Collider at CERN is used to search for the decay of a scalar boson to a pair of long-lived particles, neutral under the Standard Model gauge group, in 20.3fb−1of data collected in proton–proton collisions at √s=8TeV. This search is sensitive to long-lived particles that decay to Standard Model particles producing jets at the outer edge of the ATLAS electromagnetic calorimeter or inside the hadronic calorimeter. No significant excess of events is observed. Limits are reported on the product of the scalar boson production cross section times branching ratio into long-lived neutral particles as a function of the proper lifetime of the particles. Limits are reported for boson masses from 100 GeVto 900 GeV, and a long-lived neutral particle mass from 10 GeVto 150 GeV

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Measurement of the t(t)over-bar production cross-section using e mu events with b-tagged jets in pp collisions at root s=13 TeV with the ATLAS detector

This paper describes a measurement of the inclusive top quark pair production cross-section (sigma(t (t) over bar)) with a data sample of 3.2 fb(-1) of proton-proton collisions at a centre-of-mass energy of root s = 13 TeV, collected in 2015 by the ATLAS detector at the LHC. This measurement uses events with an opposite-charge electron-muon pair in the final state. Jets containing b-quarks are tagged using an algorithm based on track impact parameters and reconstructed secondary vertices. The numbers of events with exactly one and exactly two b-tagged jets are counted and used to determine simultaneously sigma(t (t) over bar) and the efficiency to reconstruct and b-tag a jet from a top quark decay, thereby minimising the associated systematic uncertainties. The cross-section is measured to be: s(t (t) over bar)= 818 +/- 8 (stat) +/- 27 (syst) +/- 19 (lumi) +/- 12 (beam) pb, where the four uncertainties arise from data statistics, experimental and theoretical systematic effects, the integrated luminosity and the LHC beam energy, giving a total relative uncertainty of 4.4%. The result is consistent with theoretical QCD calculations at next-to-next-to-leading order. A fiducial measurement corresponding to the experimental acceptance of the leptons is also presented. (C) 2016 The Author(s). Published by Elsevier B.V

Search for the lepton flavor violating decay Z -> e mu in pp collisions at root s=8 TeV with the ATLAS detector

The ATLAS detector at the Large Hadron Collider is used to search for the lepton flavor violating process Z -> e mu in pp collisions using 20.3 fb(-1) of data collected at root s = 8 TeV. An enhancement in the e mu invariant mass spectrum is searched for at the Z-boson mass. The number of Z bosons produced in the data sample is estimated using events of similar topology, Z -> ee and mu mu, significantly reducing the systematic uncertainty in the measurement. There is no evidence of an enhancement at the Z-boson mass, resulting in an upper limit on the branching fraction, B(Z -> e mu) < 7.5 x 10(-7) at the 95% confidence level