Experimental Study of Smoke Spread in Titled Urban Traffic Tunnels Fires

AbstractMore and more urban traffic tunnels are built due to the heavy traffic in dense urban areas. Fire safety in tunnels is a concern due to the large traffic flow. Most of the urban tunnels have slope. Knowledge on smoke spread in titled tunnel is still limited. Experimental studies on the smoke spread in a titled tunnel are carried out by the reduced-scale tunnel model tests and will be discussed in this paper. Effects of the titled gradients and longitudinal ventilation speed on the temperature distribution and smoke stratification downstream from the fire along the tunnel will be studied The results show that the smoke spread upwards much faster with the slop gradient increasing, and a thick smoke layer was formed when smoke moved to the upward part of the tunnel and filled it up. The ventilation speed had a great influence on temperature distribution along the tunnel, and the smoke stratification will be distributed when the longitudinal ventilation speed becomes large. Lower ventilation speed should be adopted at the beginning to ensure the smoke downstream of the fire keep stratified to give the tunnel users more time to escape

Association of mutation patterns in gyrA/B genes and ofloxacin resistance levels in Mycobacterium tuberculosis isolates from East China in 2009

<p>Abstract</p> <p>Background</p> <p>This study aimed to analyze the association of mutation patterns in <it>gyrA </it>and <it>gyrB </it>genes and the ofloxacin resistance levels in clinical <it>Mycobacterium tuberculosis </it>isolates sampled in 2009 from East China.</p> <p>Methods</p> <p>The quinolone resistance-determining region of <it>gyrA/B </it>were sequenced in 192 <it>M. tuberculosis </it>clinical isolates and the minimal inhibitory concentrations (MICs) of 95 ofloxacin-resistant <it>M. tuberculosis </it>isolates were determined by using microplate nitrate reductase assays.</p> <p>Results</p> <p>Mutations in <it>gyrA </it>(codons 90, 91 and 94) and in <it>gyrB </it>(G551R, D500N, T539N, R485C/L) were observed in 89.5% (85/95) and 11.6% (11/95) of ofloxacin-resistant strains, respectively. The <it>gyrB </it>mutations G551R and G549D were observed in 4.1% (4/97) of ofloxacin-susceptible strains and no mutation was found in <it>gyrA </it>in ofloxacin-susceptible strains. The MICs of all ofloxacin-resistant strains showed no significant difference among strains with mutations at codons 90, 91 or 94 in <it>gyrA </it>(F = 1.268, <it>p </it>= 0.287). No differences were detected among strains with different amino acid mutations in the quinolone resistance-determining region of <it>gyrA </it>(F = 1.877, <it>p </it>= 0.123). The difference in MICs between ofloxacin-resistant strains with mutations in <it>gyrA </it>only and ofloxacin-resistant strains with mutations in both <it>gyrA </it>and <it>gyrB </it>genes was not statistically significant (F = 0.549, <it>p </it>= 0.461).</p> <p>Conclusions</p> <p>Although <it>gyrA/B </it>mutations can lead to ofloxacin resistance in <it>M. tuberculosis</it>, there were no associations of different mutation patterns in <it>gyrA/B </it>and the level of ofloxacin resistance in <it>M. tuberculosis </it>isolates from East China in 2009.</p

Global, regional, and national burden of colorectal cancer and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Funding: F Carvalho and E Fernandes acknowledge support from Fundação para a Ciência e a Tecnologia, I.P. (FCT), in the scope of the project UIDP/04378/2020 and UIDB/04378/2020 of the Research Unit on Applied Molecular Biosciences UCIBIO and the project LA/P/0140/2020 of the Associate Laboratory Institute for Health and Bioeconomy i4HB; FCT/MCTES through the project UIDB/50006/2020. J Conde acknowledges the European Research Council Starting Grant (ERC-StG-2019-848325). V M Costa acknowledges the grant SFRH/BHD/110001/2015, received by Portuguese national funds through Fundação para a Ciência e Tecnologia (FCT), IP, under the Norma Transitória DL57/2016/CP1334/CT0006.proofepub_ahead_of_prin

The global burden of adolescent and young adult cancer in 2019 : a systematic analysis for the Global Burden of Disease Study 2019

Background In estimating the global burden of cancer, adolescents and young adults with cancer are often overlooked, despite being a distinct subgroup with unique epidemiology, clinical care needs, and societal impact. Comprehensive estimates of the global cancer burden in adolescents and young adults (aged 15-39 years) are lacking. To address this gap, we analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, with a focus on the outcome of disability-adjusted life-years (DALYs), to inform global cancer control measures in adolescents and young adults. Methods Using the GBD 2019 methodology, international mortality data were collected from vital registration systems, verbal autopsies, and population-based cancer registry inputs modelled with mortality-to-incidence ratios (MIRs). Incidence was computed with mortality estimates and corresponding MIRs. Prevalence estimates were calculated using modelled survival and multiplied by disability weights to obtain years lived with disability (YLDs). Years of life lost (YLLs) were calculated as age-specific cancer deaths multiplied by the standard life expectancy at the age of death. The main outcome was DALYs (the sum of YLLs and YLDs). Estimates were presented globally and by Socio-demographic Index (SDI) quintiles (countries ranked and divided into five equal SDI groups), and all estimates were presented with corresponding 95% uncertainty intervals (UIs). For this analysis, we used the age range of 15-39 years to define adolescents and young adults. Findings There were 1.19 million (95% UI 1.11-1.28) incident cancer cases and 396 000 (370 000-425 000) deaths due to cancer among people aged 15-39 years worldwide in 2019. The highest age-standardised incidence rates occurred in high SDI (59.6 [54.5-65.7] per 100 000 person-years) and high-middle SDI countries (53.2 [48.8-57.9] per 100 000 person-years), while the highest age-standardised mortality rates were in low-middle SDI (14.2 [12.9-15.6] per 100 000 person-years) and middle SDI (13.6 [12.6-14.8] per 100 000 person-years) countries. In 2019, adolescent and young adult cancers contributed 23.5 million (21.9-25.2) DALYs to the global burden of disease, of which 2.7% (1.9-3.6) came from YLDs and 97.3% (96.4-98.1) from YLLs. Cancer was the fourth leading cause of death and tenth leading cause of DALYs in adolescents and young adults globally. Interpretation Adolescent and young adult cancers contributed substantially to the overall adolescent and young adult disease burden globally in 2019. These results provide new insights into the distribution and magnitude of the adolescent and young adult cancer burden around the world. With notable differences observed across SDI settings, these estimates can inform global and country-level cancer control efforts. Copyright (C) 2021 The Author(s). Published by Elsevier Ltd.Peer reviewe

The global burden of cancer attributable to risk factors, 2010-19 : a systematic analysis for the Global Burden of Disease Study 2019

Background Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. Findings Globally, in 2019, the risk factors included in this analysis accounted for 4.45 million (95% uncertainty interval 4.01-4.94) deaths and 105 million (95.0-116) DALYs for both sexes combined, representing 44.4% (41.3-48.4) of all cancer deaths and 42.0% (39.1-45.6) of all DALYs. There were 2.88 million (2.60-3.18) risk-attributable cancer deaths in males (50.6% [47.8-54.1] of all male cancer deaths) and 1.58 million (1.36-1.84) risk-attributable cancer deaths in females (36.3% [32.5-41.3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20.4% (12.6-28.4) and DALYs by 16.8% (8.8-25.0), with the greatest percentage increase in metabolic risks (34.7% [27.9-42.8] and 33.3% [25.8-42.0]). Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.Peer reviewe

Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life Years for 29 Cancer Groups From 2010 to 2019: A Systematic Analysis for the Global Burden of Disease Study 2019.

The Global Burden of Diseases, Injuries, and Risk Factors Study 2019 (GBD 2019) provided systematic estimates of incidence, morbidity, and mortality to inform local and international efforts toward reducing cancer burden. To estimate cancer burden and trends globally for 204 countries and territories and by Sociodemographic Index (SDI) quintiles from 2010 to 2019. The GBD 2019 estimation methods were used to describe cancer incidence, mortality, years lived with disability, years of life lost, and disability-adjusted life years (DALYs) in 2019 and over the past decade. Estimates are also provided by quintiles of the SDI, a composite measure of educational attainment, income per capita, and total fertility rate for those younger than 25 years. Estimates include 95% uncertainty intervals (UIs). In 2019, there were an estimated 23.6 million (95% UI, 22.2-24.9 million) new cancer cases (17.2 million when excluding nonmelanoma skin cancer) and 10.0 million (95% UI, 9.36-10.6 million) cancer deaths globally, with an estimated 250 million (235-264 million) DALYs due to cancer. Since 2010, these represented a 26.3% (95% UI, 20.3%-32.3%) increase in new cases, a 20.9% (95% UI, 14.2%-27.6%) increase in deaths, and a 16.0% (95% UI, 9.3%-22.8%) increase in DALYs. Among 22 groups of diseases and injuries in the GBD 2019 study, cancer was second only to cardiovascular diseases for the number of deaths, years of life lost, and DALYs globally in 2019. Cancer burden differed across SDI quintiles. The proportion of years lived with disability that contributed to DALYs increased with SDI, ranging from 1.4% (1.1%-1.8%) in the low SDI quintile to 5.7% (4.2%-7.1%) in the high SDI quintile. While the high SDI quintile had the highest number of new cases in 2019, the middle SDI quintile had the highest number of cancer deaths and DALYs. From 2010 to 2019, the largest percentage increase in the numbers of cases and deaths occurred in the low and low-middle SDI quintiles. The results of this systematic analysis suggest that the global burden of cancer is substantial and growing, with burden differing by SDI. These results provide comprehensive and comparable estimates that can potentially inform efforts toward equitable cancer control around the world.Funding/Support: The Institute for Health Metrics and Evaluation received funding from the Bill & Melinda Gates Foundation and the American Lebanese Syrian Associated Charities. Dr Aljunid acknowledges the Department of Health Policy and Management of Kuwait University and the International Centre for Casemix and Clinical Coding, National University of Malaysia for the approval and support to participate in this research project. Dr Bhaskar acknowledges institutional support from the NSW Ministry of Health and NSW Health Pathology. Dr Bärnighausen was supported by the Alexander von Humboldt Foundation through the Alexander von Humboldt Professor award, which is funded by the German Federal Ministry of Education and Research. Dr Braithwaite acknowledges funding from the National Institutes of Health/ National Cancer Institute. Dr Conde acknowledges financial support from the European Research Council ERC Starting Grant agreement No 848325. Dr Costa acknowledges her grant (SFRH/BHD/110001/2015), received by Portuguese national funds through Fundação para a Ciência e Tecnologia, IP under the Norma Transitória grant DL57/2016/CP1334/CT0006. Dr Ghith acknowledges support from a grant from Novo Nordisk Foundation (NNF16OC0021856). Dr Glasbey is supported by a National Institute of Health Research Doctoral Research Fellowship. Dr Vivek Kumar Gupta acknowledges funding support from National Health and Medical Research Council Australia. Dr Haque thanks Jazan University, Saudi Arabia for providing access to the Saudi Digital Library for this research study. Drs Herteliu, Pana, and Ausloos are partially supported by a grant of the Romanian National Authority for Scientific Research and Innovation, CNDS-UEFISCDI, project number PN-III-P4-ID-PCCF-2016-0084. Dr Hugo received support from the Higher Education Improvement Coordination of the Brazilian Ministry of Education for a sabbatical period at the Institute for Health Metrics and Evaluation, between September 2019 and August 2020. Dr Sheikh Mohammed Shariful Islam acknowledges funding by a National Heart Foundation of Australia Fellowship and National Health and Medical Research Council Emerging Leadership Fellowship. Dr Jakovljevic acknowledges support through grant OI 175014 of the Ministry of Education Science and Technological Development of the Republic of Serbia. Dr Katikireddi acknowledges funding from a NHS Research Scotland Senior Clinical Fellowship (SCAF/15/02), the Medical Research Council (MC_UU_00022/2), and the Scottish Government Chief Scientist Office (SPHSU17). Dr Md Nuruzzaman Khan acknowledges the support of Jatiya Kabi Kazi Nazrul Islam University, Bangladesh. Dr Yun Jin Kim was supported by the Research Management Centre, Xiamen University Malaysia (XMUMRF/2020-C6/ITCM/0004). Dr Koulmane Laxminarayana acknowledges institutional support from Manipal Academy of Higher Education. Dr Landires is a member of the Sistema Nacional de Investigación, which is supported by Panama’s Secretaría Nacional de Ciencia, Tecnología e Innovación. Dr Loureiro was supported by national funds through Fundação para a Ciência e Tecnologia under the Scientific Employment Stimulus–Institutional Call (CEECINST/00049/2018). Dr Molokhia is supported by the National Institute for Health Research Biomedical Research Center at Guy’s and St Thomas’ National Health Service Foundation Trust and King’s College London. Dr Moosavi appreciates NIGEB's support. Dr Pati acknowledges support from the SIAN Institute, Association for Biodiversity Conservation & Research. Dr Rakovac acknowledges a grant from the government of the Russian Federation in the context of World Health Organization Noncommunicable Diseases Office. Dr Samy was supported by a fellowship from the Egyptian Fulbright Mission Program. Dr Sheikh acknowledges support from Health Data Research UK. Drs Adithi Shetty and Unnikrishnan acknowledge support given by Kasturba Medical College, Mangalore, Manipal Academy of Higher Education. Dr Pavanchand H. Shetty acknowledges Manipal Academy of Higher Education for their research support. Dr Diego Augusto Santos Silva was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil Finance Code 001 and is supported in part by CNPq (302028/2018-8). Dr Zhu acknowledges the Cancer Prevention and Research Institute of Texas grant RP210042

Microwave absorption and antioxidation properties of flaky carbonyl iron passivated with carbon dioxide

Carbonyl iron particle is a typical magnetic microwave absorbing material. Because of the effect of particle shape, the flaky carbonyl iron has large values of microwave permeability and can be an excellent super-thin absorber. However, the flaky carbonyl iron prepared by high-energy ball milling has high activity and is apt to be oxidized. Based on a reverse reaction of the blast furnace iron-making process, this work developed a facile passivation method with carbon dioxide to improve the antioxidation property of the flaky carbonyl iron. The antioxidation property of the passivated carbonyl iron was improved greatly while the excellent microwave absorption property maintained. (C) 2013 Elsevier B.V. All rights reserved

Field and laboratory screening of anthurium cultivars for resistance to foliar bacterial blight and the induced activities of defence-related enzymes

Bacterial blight (BB) caused by Xanthomonas axonopodis pv. dieffenbachiae (Xad) is the most destructive disease of ornamental anthurium. In the present study, foliar resistance of 21 anthurium cultivars were assessed under shaded field and laboratory conditions by injection inoculation of 3 × 108 cfu/ml Xad; disease severity was evaluated using a pretransformed rating scale after symptoms survey. Then six selected cultivars with different resistance levels were evaluated for the induced activities of six defence-related enzymes. The obtained results indicated that the same cultivar shared identical resistance under both conditions, but there was a great variation among the cultivars. Anthurium cv. Pink Champion and Manaka showed the highest resistance, and five other cultivars were highly susceptible. The activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), peroxidase (POD) and phenylalanine ammonia-lyase (PAL) in the resistant cultivars increased much faster and reached much higher peak levels than those in susceptible cultivars. Further analyses revealed that the relative resistance index (RRI) significantly positively correlated with the activities of SOD, APX, POD and PAL, but not with catalase (CAT) and polyphenol oxidase (PPO), suggesting that early rapid accumulation of SOD, APX, PAL and POD might be an important mechanism of defence against Xad and could serve as one of the valuable physiological indices for the prediction of BB resistance in anthurium germplasm. Consequently, the identified resistant cultivars and the induced defence enzymes will facilitate the phytopathological research and enhance blight resistance selection in future breeding

Synthesis of hollow carbonyl iron microspheres via pitting corrosion method and their microwave absorption properties

In this paper, we report a new method to prepare hollow carbonyl iron microspheres, which is called pitting corrosion method. The comparison of the morphology, specific surface area and apparent density of the initial and pitting corroded carbonyl iron microspheres demonstrate that the pitting corroded carbonyl iron has a hollow structure. The pitting corrosion process is uncovered through the concentration change of ferrous ion in the reaction solution and the TEM images with different pitting corrosion time. The formation mechanism of hollow microspheres via pitting corrosion is analyzed. Furthermore, this pitting corrosion method can also be used to prepare other hollow metal particles, such as Ni, Co, and Cu particles. The electromagnetic parameters of the samples before and after pitting corrosion are measured. The calculated reflection loss of the pitting corroded sample for single layer of 0.5 mm or 1.0 mm thickness at 2-18 GHz is much better than that of the initial one. The mechanism of the improvement of the microwave absorption properties is discussed. (c) 2013 Elsevier B.V. All rights reserved

Partial DNA-guided Cas9 enables genome editing with reduced off-target activity

CRISPR-Cas9 is a versatile RNA-guided genome editing tool. Here we demonstrate that partial replacement of RNA nucleotides with DNA nucleotides in CRISPR RNA (crRNA) enables efficient gene editing in human cells. This strategy of partial DNA replacement retains on-target activity when used with both crRNA and sgRNA, as well as with multiple guide sequences. Partial DNA replacement also works for crRNA of Cpf1, another CRISPR system. We find that partial DNA replacement in the guide sequence significantly reduces off-target genome editing through focused analysis of off-target cleavage, measurement of mismatch tolerance and genome-wide profiling of off-target sites. Using the structure of the Cas9-sgRNA complex as a guide, the majority of the 3′ end of crRNA can be replaced with DNA nucleotide, and the 5 - and 3′-DNA-replaced crRNA enables efficient genome editing. Cas9 guided by a DNA-RNA chimera may provide a generalized strategy to reduce both the cost and the off-target genome editing in human cells.National Institutes of Health (U.S.) (5-U54-CA151884-04)Skoltech-MIT Center for Electrochemical EnergyNational Institutes of Health (U.S.) (Cancer Center Support (core) grant P30-CA14051