66 research outputs found

    Corrosion: how to control it?

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    PFC presentat a Oslo University College and Oslo Heart CenterTreball desenvolupat dins el marc del programa 'European Project Semester'.Established in 1989, Oslo Heart Centre (OHC) is located in downtown Oslo, Norway. The hospital is a non-profit cardiac surgical clinic. To control the temperature in the hospital during the summer months, an air-conditioning system is installed. The ten years old air-conditioning system suffers from corrosion problems, inside and outside stainless steel pipes. The aim of this project is to find solutions in order to reduce the amount of corrosion. Heat loss due to an insufficient insulation, contamination and erosion are secondary, indirect problems. To analyze the situation, various measurements were performed such as, pipe thickness (amount of corrosion), humidity and water quality. It appeared that: · The pipes thickness is decreased with 0,7 mm due to corrosion. · The humidity is 100%, for both inside and around the insulation. · The pH value (pH = 8) and the amount of iron parts (0,15 mg/kg) are not within the boundaries of the recommended values. Moreover the measured O2 level is misleading. After an inspection concerning the existing conditions, the problems were defined and organized by priority. The main problem is corrosion which occurs due to three sub-problems: · A too high O2 level in the water-glycol mix, which provokes rust by a chemical reaction. · Uninhibited glycol which turns sour in acids by reacting with the metal pipes. · Insufficient insulation which provokes water vapour condensation at the pipes surface. To control these problems, the following solutions have been suggested: · Reduce the O2 level. · Remove the glycol and replace it with a product which contains inhibiters against corrosion. · Change the old insulation and replace it with a more water vapour resistant insulation. After several comparisons of different techniques, products, environmental consequences and an economic analysis based on a ten years period, solutions for each problem are suggested: · Add H2 to the water-glycol mix to form a chemical reaction with O2. A system provided by the Norwegian company Niprox® (costs: less than 2000 €/year). · Replace the glycol with an inhibited propylene glycol (costs: less than 10000 €/year). · Use Armaflex® foam sheets as insulation outside the pipes, for a better resistance against water vapour. (cost: about 5000 €/year) With all these alternatives, the OHC could reduce the amount of corrosion within the air-conditioning system

    Reduced physiological performance in a free-living coralline alga induced by salmon faeces deposition

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    Maerl beds are formed by the accumulation of free-living coralline algae and have considerable ecological significance due to the high diversity of associated fauna and flora. The rapid expansion of the Atlantic salmon Salmo salar aquaculture industry in Norway may have major impacts on surrounding maerl beds through the release of effluents, including fish faeces. This study is the first to test the effects of salmon faeces and inorganic sediment deposition on the photosynthesis, respiration, calcification and pigment content of the coralline alga Lithothamnion soriferum. In a 6 wk laboratory experiment, inorganic sediment and salmon faeces deposition significantly reduced the amount of light reaching the surface of coralline algae. No impact of inorganic sediment deposition was detected on L. soriferum physiology, while salmon faeces deposition increased respiration rate and reduced net primary production and calcification. The accumulation of salmon faeces stimulates proliferation of bacteria, with adverse consequences on L. soriferum physiology due to the potential release of toxic compounds. Burial by salmon faeces deposition also affects the physiology of coralline algae due to the flocculation of sticky faeces particles, which may limit nutrient and gas exchanges in the vicinity of thalli. Carbon dioxide accumulation in the vicinity of L. soriferum may lead to a decline in pH and alter the calcification process in cell walls. In natural maerl beds, the negative effect of faeces deposition may be exacerbated by longer-term exposure and the presence of other chemicals released by fish farms.publishedVersio

    Equine herpesvirus diseases: relevance and limits of molecular tools

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    At least five equine herpesviruses are known to infect horses: three alpha herpesviruses (equine herpesvirus- 1, -3 and -4) and two gamma herpesviruses (equine herpesvirus-2 and -5). Equine herpesvirus- 1 is responsible for three clinical presentations: respiratory, abortigenic and neurological. This latter, widely known as EHV-1 associated, myeloencephalopathy has been thoroughly investigated over the past years. Most of the studies focused on the relation between the presence of a mutation in ORF 30 coding for DNA polymerase and the expression of the paralytic (neurological) form. Even if this mutation seems to play a role, other factors related to the host and the environment are certainly involved in the development of the disease. Equine herpesvirus-4 is better known as the rhinopneumonia virus and is responsible for a large part of respiratory disorders in young foals. Equine herpesvirus- 3 is responsible for equine coital exanthema, whose transmission through the respiratory tract is now proven. Equine herpesvirus-2 and -5 are associated with subclinical respiratory diseases in equine athletes, even though their pathogenic role has yet to be clarified as they were detected in all continents only relatively recently. The development of molecular genetic tools lead to major progress in the detection of these viruses, but the differentiation between latent and infectious forms is still unresolved. Although studies are currently performed on the typing of strains responsible for different clinical presentations involving equine herpesviruses as well as in other equine viruses (influenza, equine viral arteritis), there is no international consensus on a phylogenic tree for any of the 5 equine herpesviruses. Further studies are definitely required to monitor and characterise the different strains of EHV.Au moins cinq herpèsvirus équins peuvent infecter le cheval: trois alpha-herpèsvirus (les herpèsvirus 1, 3 et 4) et deux gamma-herpèsvirus (les herpèsvirus équins 2 et 5). L'herpèsvirus équin 1 est responsable de trois formes cliniques: une forme respiratoire, une forme abortive et une forme neurologique. Cette dernière, plus connue sous le nom de myéloencéphalopathie à HVE-1, a fait l'objet de nombreuses études ces dernières années. La plupart des travaux ont porté sur la relation entre la présence d'une mutation dans l'ORF 30 codant l'ADN polymérase et l'expression de la forme paralytique. Si cette mutation semble jouer un rôle, d'autres facteurs liés à l'hôte et à l'environnement participent certainement au développement de la maladie. L'herpèsvirus équin 4 est plus connu sous le nom de virus de la rhinopneumonie et est responsable d'une part importante des affections respiratoires chez les jeunes poulains. L'herpèsvirus équin 3 est responsable de l'exanthème coïtal équin et l'on sait aujourd'hui qu'il peut se transmettre par les voies respiratoires. Les herpèsvirus équins 2 et 5 sont associés aux maladies respiratoires subcliniques du cheval athlète même si leur rôle reste à préciser, leur découverte sur l'ensemble des continents étant relativement récente. Le développement des outils de génétique moléculaire a permis de faire des progrès importants dans la détection de ces virus même si un challenge demeure: différencier les formes latentes des formes infectieuses. Si comme pour d'autres virus équins (ex: grippe, artérite virale équine), des travaux sont réalisés pour typer les différentes souches responsables de différentes formes d'expression de la maladie, il n'existe toujours pas de consensus international sur un arbre phylogénique pour aucun de ces cinq herpèsvirus équins. Le suivi et la caractérisation des différentes souches d'HVEs sont très certainement l'autre défi de demain

    Strong HIV-1-Specific T Cell Responses in HIV-1-Exposed Uninfected Infants and Neonates Revealed after Regulatory T Cell Removal

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    BACKGROUND: In utero transmission of HIV-1 occurs on average in only 3%–15% of HIV-1-exposed neonates born to mothers not on antiretroviral drug therapy. Thus, despite potential exposure, the majority of infants remain uninfected. Weak HIV-1-specific T-cell responses have been detected in children exposed to HIV-1, and potentially contribute to protection against infection. We, and others, have recently shown that the removal of CD4(+)CD25(+) T-regulatory (Treg) cells can reveal strong HIV-1 specific T-cell responses in some HIV-1 infected adults. Here, we hypothesized that Treg cells could suppress HIV-1-specific immune responses in young children. METHODOLOGY/PRINCIPAL FINDINGS: We studied two cohorts of children. The first group included HIV-1-exposed-uninfected (EU) as well as unexposed (UNEX) neonates. The second group comprised HIV-1-infected and HIV-1-EU children. We quantified the frequency of Treg cells, T-cell activation, and cell-mediated immune responses. We detected high levels of CD4(+)CD25(+)CD127(−) Treg cells and low levels of CD4(+) and CD8(+) T cell activation in the cord blood of the EU neonates. We observed HIV-1-specific T cell immune responses in all of the children exposed to the virus. These T-cell responses were not seen in the cord blood of control HIV-1 unexposed neonates. Moreover, the depletion of CD4(+)CD25(+) Treg cells from the cord blood of EU newborns strikingly augmented both CD4(+) and CD8(+) HIV-1-specific immune responses. CONCLUSIONS/SIGNIFICANCE: This study provides new evidence that EU infants can mount strong HIV-1-specific T cell responses, and that in utero CD4(+)CD25(+) T-regulatory cells may be contributing to the lack of vertical transmission by reducing T cell activation

    Estimating global injuries morbidity and mortality : methods and data used in the Global Burden of Disease 2017 study

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    Background While there is a long history of measuring death and disability from injuries, modern research methods must account for the wide spectrum of disability that can occur in an injury, and must provide estimates with sufficient demographic, geographical and temporal detail to be useful for policy makers. The Global Burden of Disease (GBD) 2017 study used methods to provide highly detailed estimates of global injury burden that meet these criteria. Methods In this study, we report and discuss the methods used in GBD 2017 for injury morbidity and mortality burden estimation. In summary, these methods included estimating cause-specific mortality for every cause of injury, and then estimating incidence for every cause of injury. Non-fatal disability for each cause is then calculated based on the probabilities of suffering from different types of bodily injury experienced. Results GBD 2017 produced morbidity and mortality estimates for 38 causes of injury. Estimates were produced in terms of incidence, prevalence, years lived with disability, cause-specific mortality, years of life lost and disability-adjusted life-years for a 28-year period for 22 age groups, 195 countries and both sexes. Conclusions GBD 2017 demonstrated a complex and sophisticated series of analytical steps using the largest known database of morbidity and mortality data on injuries. GBD 2017 results should be used to help inform injury prevention policy making and resource allocation. We also identify important avenues for improving injury burden estimation in the future.Peer reviewe

    Global injury morbidity and mortality from 1990 to 2017 : results from the Global Burden of Disease Study 2017

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    Correction:Background Past research in population health trends has shown that injuries form a substantial burden of population health loss. Regular updates to injury burden assessments are critical. We report Global Burden of Disease (GBD) 2017 Study estimates on morbidity and mortality for all injuries. Methods We reviewed results for injuries from the GBD 2017 study. GBD 2017 measured injury-specific mortality and years of life lost (YLLs) using the Cause of Death Ensemble model. To measure non-fatal injuries, GBD 2017 modelled injury-specific incidence and converted this to prevalence and years lived with disability (YLDs). YLLs and YLDs were summed to calculate disability-adjusted life years (DALYs). Findings In 1990, there were 4 260 493 (4 085 700 to 4 396 138) injury deaths, which increased to 4 484 722 (4 332 010 to 4 585 554) deaths in 2017, while age-standardised mortality decreased from 1079 (1073 to 1086) to 738 (730 to 745) per 100 000. In 1990, there were 354 064 302 (95% uncertainty interval: 338 174 876 to 371 610 802) new cases of injury globally, which increased to 520 710 288 (493 430 247 to 547 988 635) new cases in 2017. During this time, age-standardised incidence decreased non-significantly from 6824 (6534 to 7147) to 6763 (6412 to 7118) per 100 000. Between 1990 and 2017, age-standardised DALYs decreased from 4947 (4655 to 5233) per 100 000 to 3267 (3058 to 3505). Interpretation Injuries are an important cause of health loss globally, though mortality has declined between 1990 and 2017. Future research in injury burden should focus on prevention in high-burden populations, improving data collection and ensuring access to medical care.Peer reviewe

    Corrosion: how to control it?

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    PFC presentat a Oslo University College and Oslo Heart CenterTreball desenvolupat dins el marc del programa 'European Project Semester'.Established in 1989, Oslo Heart Centre (OHC) is located in downtown Oslo, Norway. The hospital is a non-profit cardiac surgical clinic. To control the temperature in the hospital during the summer months, an air-conditioning system is installed. The ten years old air-conditioning system suffers from corrosion problems, inside and outside stainless steel pipes. The aim of this project is to find solutions in order to reduce the amount of corrosion. Heat loss due to an insufficient insulation, contamination and erosion are secondary, indirect problems. To analyze the situation, various measurements were performed such as, pipe thickness (amount of corrosion), humidity and water quality. It appeared that: · The pipes thickness is decreased with 0,7 mm due to corrosion. · The humidity is 100%, for both inside and around the insulation. · The pH value (pH = 8) and the amount of iron parts (0,15 mg/kg) are not within the boundaries of the recommended values. Moreover the measured O2 level is misleading. After an inspection concerning the existing conditions, the problems were defined and organized by priority. The main problem is corrosion which occurs due to three sub-problems: · A too high O2 level in the water-glycol mix, which provokes rust by a chemical reaction. · Uninhibited glycol which turns sour in acids by reacting with the metal pipes. · Insufficient insulation which provokes water vapour condensation at the pipes surface. To control these problems, the following solutions have been suggested: · Reduce the O2 level. · Remove the glycol and replace it with a product which contains inhibiters against corrosion. · Change the old insulation and replace it with a more water vapour resistant insulation. After several comparisons of different techniques, products, environmental consequences and an economic analysis based on a ten years period, solutions for each problem are suggested: · Add H2 to the water-glycol mix to form a chemical reaction with O2. A system provided by the Norwegian company Niprox® (costs: less than 2000 €/year). · Replace the glycol with an inhibited propylene glycol (costs: less than 10000 €/year). · Use Armaflex® foam sheets as insulation outside the pipes, for a better resistance against water vapour. (cost: about 5000 €/year) With all these alternatives, the OHC could reduce the amount of corrosion within the air-conditioning system

    EHV-4 Reloaded (Data update)

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    International audienceEquine rhinopneumonitis, caused by Equid Herpesvirus 4 (EHV-4) and EHV-1, is one of the most frequent respiratory diseases experienced by horse breeders and trainers. The French equine infectious diseases surveillance network (RESPE) reports numerous outbreaks each year, which can significantly disrupt economic activities, as illustrated in France in 2018 when more than 200 equestrian events were cancelled. While the origin of this crisis could date back from the 2016 EHV vaccine shortage, no scientific evidence has been obtained to date.Research teams have often been less interested in the study of EHV-4, probably because EHV-1 is known to induce more severe forms of diseases (i.e. abortions, neonatal deaths and myeloencephalopathy). However, EHV-4 is responsible for approximately 6 times more epizootics (respiratory infection) than EHV-1 (1,2). Several cases of EHV-4 induced abortion have also been observed and reported in recent years (3,4).All of these data attest to the importance of the pathology associated with HVE-4 infection and demonstrate the need to better characterizing EHV-4 common characteristics and differencies with EHV-1.The objectives of this new project are to : 1 / Understand the importance of EHV-4 during the 2018 French crisis in a degraded context of vaccination.2 /Characterise EHV-4 infection in order to improve pathophysiology knowledge, an essential step for future and effective prophylaxis.3 / Characterise EHV-4 strains at the molecular level to identify future vaccine and antiviral targets

    EHV-4 Reloaded (Data update)

    No full text
    International audienceEquine rhinopneumonitis, caused by Equid Herpesvirus 4 (EHV-4) and EHV-1, is one of the most frequent respiratory diseases experienced by horse breeders and trainers. The French equine infectious diseases surveillance network (RESPE) reports numerous outbreaks each year, which can significantly disrupt economic activities, as illustrated in France in 2018 when more than 200 equestrian events were cancelled. While the origin of this crisis could date back from the 2016 EHV vaccine shortage, no scientific evidence has been obtained to date.Research teams have often been less interested in the study of EHV-4, probably because EHV-1 is known to induce more severe forms of diseases (i.e. abortions, neonatal deaths and myeloencephalopathy). However, EHV-4 is responsible for approximately 6 times more epizootics (respiratory infection) than EHV-1 (1,2). Several cases of EHV-4 induced abortion have also been observed and reported in recent years (3,4).All of these data attest to the importance of the pathology associated with HVE-4 infection and demonstrate the need to better characterizing EHV-4 common characteristics and differencies with EHV-1.The objectives of this new project are to : 1 / Understand the importance of EHV-4 during the 2018 French crisis in a degraded context of vaccination.2 /Characterise EHV-4 infection in order to improve pathophysiology knowledge, an essential step for future and effective prophylaxis.3 / Characterise EHV-4 strains at the molecular level to identify future vaccine and antiviral targets
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