Experimental investigation of the effects of simultaneous hydrogen and nitrogen addition on the emissions and combustion of a diesel engine

This article is made available through the Brunel Open Access Publishing Fund. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited. Copyright @ 2013, Hydrogen Energy Publications, LLC. Published by Elsevier Ltd. All rights reserved.Overcoming diesel engine emissions trade-off effects, especially NO and Bosch smoke number (BSN), requires investigation of novel systems which can potentially serve the automobile industry towards further emissions reduction. Enrichment of the intake charge with H + N containing gas mixture, obtained from diesel fuel reforming system, can lead to new generation low polluting diesel engines. This paper investigates the effect of simultaneous H + N intake charge enrichment on the emissions and combustion of a compression ignition engine. Bottled H + N was simultaneously admitted into the intake pipe of the engine in 4% steps starting from 4% (2% H + 2% N) up to 16% (v/v). The results showed that under specific operating conditions H + N enrichment can offer simultaneous NO, BSN and CO emissions reduction. Apart from regulated emissions, nitrogen exhaust components were measured. Marginal NO and zero NH emissions were obtained. NO/NO ratio increases when speed or load increases. Under low speed low load operation the oxidation of NO is enhanced by the addition of H + N mixture. Finally, admission of H + N has a detrimental effect on fuel consumption.UK Engineering and Physical Science Research Counci

Tobacco Smoke: Involvement of Reactive Oxygen Species and Stable Free Radicals in Mechanisms of Oxidative Damage, Carcinogenesis and Synergistic Effects with Other Respirable Particles

Tobacco smoke contains many toxic, carcinogenic and mutagenic chemicals, as well as stable and unstable free radicals and reactive oxygen species (ROS) in the particulate and the gas phase with the potential for biological oxidative damage. Epidemiological evidence established that smoking is one of the most important extrinsic factor of premature morbidity and mortality. The objective of this study was to investigate oxidative and carcinogenic mechanisms of tobacco and synergistic action with other respirable particles in the respiratory system of smokers. Electron Paramagnetic Resonance (EPR) and spin-trapping techniques were used to study stable free radicals in the cigarette tar, and unstable superoxide anion (O2•−) and hydroxyl (HO•) radicals in the smoke Results showed that the semiquinone radical system has the potential for redox recycling and oxidative action. Further, results proved that aqueous cigarette tar (ACT) solutions can generate adducts with DNA nucleobases, particularly the mutagenic 8-hydroxy-2’-deoxyguanosine (a biomarker for carcinogenesis). Also, we observed synergistic effects in the generation of HO•, through the Fenton reaction, with environmental respirable particles (asbestos fibres, coal dust, etc.) and ambient particulate matter (PM), such as PM10, PM2.5 and diesel exhaust particles (DEP). The highest synergistic effects was observed with the asbestos fibres (freshly grounded), PM2.5 and DEP. Finally, we discuss results from our previous study of conventional cellulose acetate filters and “bio-filters” with hemoglobin impregnated activated carbon, which showed that these filters do not substantially alter the free radical content of smoke in the particulate and in the gaseous phase

Epidemics of Infectious Diseases in Human History. Antiviral Drugs and Vaccines in the Development Stage to Protect Against Coronavirus SARS-CoV-2

Abstract. Infectious diseases have plagued humanity since the earliest days of civilizations. Civilizations and subsequent history have been altered profoundly by the outbreak of pathogenic infectious diseases that decimated societies and killed millions of people. The formation of agrarian communities facilitated and increased the spread of infectious diseases. Widespread trade created new opportunities for human and animal interactions that sped up such epidemics. Malaria, tuberculosis, leprosy, smallpox, influenza, smallpox, cholera, viruses and other infectious agents appeared during these early years. Urbanization, expansion of cities, globalization of trade and the explosion of mass international travelling increased contact with different populations of people, animals, and ecosystems. All these factors contributed to old and recent infectious disease pandemics. Vaccination is widely considered one of the greatest medical achievements of modern human civilization. Infectious diseases that were commonplace less than a generation ago are now increasingly rare because of vaccines and various antiviral drugs. The current outbreak of the pandemic of virus SARS-CoV-2 (2019-2020) caught developed and developing countries with widespread sickness and deaths. At the same time it initiated an urgent need by big pharmaceutical companies and research centers of medical institutions worldwide to search for new drugs and vaccines to combat the new virulent coronavirus. The virus has been proved to be very contagious and has already shown it has the potential to kill people like the elderly and people with underlying health conditions. This review covers all the recent developments all over the world for antiviral pharmaceutical agents and suitable vaccines. Also, the World Health Organization (WHO) announced in March 2020 a large global trial, called SOLIDARITY, to find out if can treat infections like COVID-19 coronavirus. It is an unprecedented effort—an all-out, coordinated push to collect robust scientific data rapidly during a pandemic. Also, the European community initiates the DISCOVERY project to include 3,200 European patients from Belgium, France, Germany Luxembourg, the Netherlands, Spain, Sweden, and the United Kingdom. In France, at least 800 hospitalized COVID-19 patients will be recruited

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM10 and PM2.5) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis

Determination of selective quinones and quinoid radicals in airborne particulate matter and vehicular exhaust particles (vol 3, pg 118, 2006)

In recent years, there has been an increasing interest in the study of the health effects of respirable particulate matter ( PM) because of its deposition in the human lungs and adverse health effects. Analysis of PM content focused on substances of toxicological importance, such as polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, aliphatic hydrocarbons, alkyl-substituted benzenes and naphthalenes, transition metals and various quinones. Recent studies shifted their attention to quinones and their toxicological role in PM. Quinones can be transformed into their semiquinones, which undergo redox cycling and reduce oxygen to produce reactive oxygen species (ROS) in biological systems, resulting in the induction of oxidative stress, especially oxidative damage to cellular components and DNA. In the present study, the presence of five quinones, 1,2-benzenediol ( catechol) and 1,4-benzenediol ( hydroquinone) in various PM samples was identified and measured quantitatively by high performance liquid chromatography. Mean concentrations of individual target quinones ranged from 15 140 ng mg(-1) in diesel and gasoline exhaust particles to 1.5-60 ng mg(-1) (or 150-1100 pg m(-3)) in airborne PM ( total suspended particulates, PM aerodynamic diameter 10 mu m, PM aerodynamic diameter 2.1 mu m) samples. Precision (repeatability and reproducibility) varied from 5 to 15%. Also, examples of electron paramagnetic resonance spectra for the single broad unstructured signal are presented, corresponding to the persistent stable semiquinone radicals of solid samples of PM, and the formation of quinoid radicals in aqueous extracts of PM samples in air-saturated carbonate-buffered solution, pH 9.5-10

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM10 and PM2.5) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis