Study of the anticorrosive properties on SAE 1010 steel of rosemary (Rosmarinus officinalis), laurel (Laurus nobilis) and false incense (Plectranthus coleoides)

Las hojas de las plantas perennes Rosmarinus officinalis, Laurus nobilis y Plectranthus coleoides presentan una gran cantidad de compuestos químicos que contienen heteroátomos en su estructura. Diversos estudios han reportado que este tipo de heterocompuestos presentan una gran afinidad química por las superficies metálicas. En este trabajo se presenta la obtención, caracterización y estudio del desempeño anticorrosivo sobre acero SAE 1010 de los extractos acuosos de las hojas de las plantas perennes antes mencionadas. Las especies vegetales fueron cultivadas y cosechadas en la zona del Gran La Plata, Provincia de Buenos Aires, República Argentina. La preparación de los extractos acuosos se realizó mediante la técnica de maceración.El residuo sólido de los extractos acuosos se caracterizó mediante espectroscopia infrarroja con transformada de Fourier (FTIR). La evaluación electroquímica se llevó a cabo mediante la exposición de muestras de acero SAE 1010 durante 24 h a un medio corrosivo en presencia de cada uno de los extractos, y el posterior análisis de las superficies obtenidas a través de microscopía electrónica de barrido (SEM) y espectroscopia de dispersión de rayos X (EDX). Los resultados fueron comparados con los obtenidos utilizando hidrato de polifosfato de zinc y aluminio (ZAPP), un pigmento anticorrosivo comercial. Los resultados obtenidos permiten concluir que los extractos de las tres especies vegetales inhiben la corrosión del acero SAE 1010 de manera comparable a la efectuada por ZAPP, siendo el extracto de Plectranthus coleoides el que presenta la mejor acción anticorrosiva.The leaves of perennials plants Rosmarinus officinalis, Laurus nobilis and Plectranthus coleoides have a large number of chemical compounds that contain heteroatoms in their structure. This type of heterocompounds has been reported to have chemical affinity for metal surfaces. This work presents the obtaining, characterization and study of the anticorrosive performance on SAE 1010 steel of the aqueous extracts of the aforementioned perennials plants. The plant species were cultivated and harvested in the Greater La Plata area, Province of Buenos Aires, Argentine Republic. The preparation of the aqueous extracts was carried out using the maceration technique. The solid residue of the aqueous extracts was characterized by Fourier transform infrared spectroscopy (FTIR). Electrochemical evaluation was accomplished by linear polarization tests. The anticorrosive performance was determined by exposing SAE 1010 steel samples for 24 h to a corrosive medium in the presence of each of the extracts, and the subsequent analysis of the surfaces obtained through scanning electron microscopy (SEM) and X-ray scattering spectroscopy (EDX). The results were compared with those obtained using zinc aluminum polyphosphate hydrate (ZAPP), a commercial anticorrosive pigment. The results obtained allow us to conclude that the extracts of the three plants inhibit the corrosion of SAE 1010 steel in a manner comparable to that carried out by ZAPP, with the extract of Plectranthus coleoides being the one that presents the best anticorrosive action.Fil: Byrne, Christian Eduardo. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Centro de Investigaciones en Tecnología de Pinturas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones en Tecnología de Pinturas; ArgentinaFil: Martin Ramirez, Mariano Esteban. Universidad Tecnologica Nacional. Facultad Regional La Plata; ArgentinaFil: Di Santo, Ezequiel. Universidad Tecnologica Nacional. Facultad Regional La Plata; ArgentinaFil: Cristiano, Nicol. Universidad Tecnologica Nacional. Facultad Regional La Plata; ArgentinaFil: Deya, Marta Cecilia. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Centro de Investigaciones en Tecnología de Pinturas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones en Tecnología de Pinturas; ArgentinaFil: D'alessandro, Oriana. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Centro de Investigaciones en Tecnología de Pinturas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones en Tecnología de Pinturas; Argentin

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome : Insights from the LUNG SAFE study

Publisher Copyright: © 2020 The Author(s). Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Background: Concerns exist regarding the prevalence and impact of unnecessary oxygen use in patients with acute respiratory distress syndrome (ARDS). We examined this issue in patients with ARDS enrolled in the Large observational study to UNderstand the Global impact of Severe Acute respiratory FailurE (LUNG SAFE) study. Methods: In this secondary analysis of the LUNG SAFE study, we wished to determine the prevalence and the outcomes associated with hyperoxemia on day 1, sustained hyperoxemia, and excessive oxygen use in patients with early ARDS. Patients who fulfilled criteria of ARDS on day 1 and day 2 of acute hypoxemic respiratory failure were categorized based on the presence of hyperoxemia (PaO2 > 100 mmHg) on day 1, sustained (i.e., present on day 1 and day 2) hyperoxemia, or excessive oxygen use (FIO2 ≥ 0.60 during hyperoxemia). Results: Of 2005 patients that met the inclusion criteria, 131 (6.5%) were hypoxemic (PaO2 < 55 mmHg), 607 (30%) had hyperoxemia on day 1, and 250 (12%) had sustained hyperoxemia. Excess FIO2 use occurred in 400 (66%) out of 607 patients with hyperoxemia. Excess FIO2 use decreased from day 1 to day 2 of ARDS, with most hyperoxemic patients on day 2 receiving relatively low FIO2. Multivariate analyses found no independent relationship between day 1 hyperoxemia, sustained hyperoxemia, or excess FIO2 use and adverse clinical outcomes. Mortality was 42% in patients with excess FIO2 use, compared to 39% in a propensity-matched sample of normoxemic (PaO2 55-100 mmHg) patients (P = 0.47). Conclusions: Hyperoxemia and excess oxygen use are both prevalent in early ARDS but are most often non-sustained. No relationship was found between hyperoxemia or excessive oxygen use and patient outcome in this cohort. Trial registration: LUNG-SAFE is registered with ClinicalTrials.gov, NCT02010073publishersversionPeer reviewe

Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

Correction to: Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

The original version of this article unfortunately contained a mistake

Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

Diminished Fluid Transport through Carbon Nanochannels Induced by COOH Functionalization: Implications for Nanofiltration and Oil Recovery

Fluid transport on confined systems is a subject of theoretical and technological interest. For instance, remarkable high flow rates have been obtained in carbon nanochannels (CNs) which cannot be predicted by standard macroscopic theories. Natural rocks, which are at the heart of the shale hydrocarbon revolution, may also exhibit similar properties as the porous structure is mainly at the nanoscale and is carbon rich. Among other differences with CNs, the surfaces are not atomically smooth, as they have organic functional groups anchored on their inner porous surfaces. In this work, we assess the effects of carboxylic functionalization of the nanochannel surfaces on fluid transport. We consider water and methane as representative cases for polar/non-polar fluids and also mixtures of them. We find that the presence of only a few carboxylic groups on the CN causes a large reduction of flow rates for all fluids considered due to the associated geometrical distortion. However, for water, the hydrophilicity induced by the carboxylic functionalization causes not only a dramatic reduction in flow rates but also structural changes in which COOH groups act as nucleation centers for water droplets. Implications of our results show that the flow rates depend on the O/C ratio of the nanochannel, which is a measure of kerogen maturity. The relationship between rock permeability and maturity may provide a way to identify high conductive zones for hydrocarbon recovery. Another application is the possible use of chemical additives to enhance hydrocarbon flow on kerogen-rich rocks. The presence of a small amount of scattered organic functional groups in the nanochannel helps to distribute water molecules along the nanochannel walls, opening a path for hydrocarbon to flow.Fil: Martin Ramirez, Mariano Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. YPF - Tecnología; Argentina. Universidad Nacional de La Plata. Facultad de Ingeniería; ArgentinaFil: Gil Sánchez, Mariela Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Simulación Computacional para Aplicaciones Tecnológicas; Argentina. Universidad Nacional de San Martín; ArgentinaFil: Castez, Marcos Federico. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. YPF - Tecnología; Argentina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Matemáticas; ArgentinaFil: Winograd, Emilio Andres. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. YPF - Tecnología; Argentin

The genome sequence of Trypanosoma cruzi, etiologic agent of Chagas disease

Fil: El-Sayed, Najib M. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Myler, Peter J. Seattle Biomedical Research Institute; Estados Unidos.Fil: Bartholomeu, Daniella C. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Nilsson, Daniel. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Aggarwal, Gautam. Seattle Biomedical Research Institute; Estados Unidos.Fil: Tran, Anh-Nhi. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Ghedin, Elodie. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Worthey, Elizabeth A. Seattle Biomedical Research Institute; Estados Unidos.Fil: Delcher, Arthur L. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Blandin, Gaëlle. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Westenberger, Scott J. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Caler, Elisabet. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Cerqueira, Gustavo C. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Haas, Carole Branched Brian. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Anupama, Atashi. Seattle Biomedical Research Institute; Estados Unidos.Fil: Arner, Erik. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Åslund, Lena. Uppsala University. Department of Genetics and Pathology; Suecia.Fil: Attipoe, Philip. Seattle Biomedical Research Institute; Estados Unidos.Fil: Bontempi, Esteban. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Bringaud, Frédéric. Université Victor Segalen Bordeaux II. Laboratoire de Génomique Fonctionnelle des Trypanosomatides; Francia.Fil: Burton, Peter. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: Cadag, Eithon. Seattle Biomedical Research Institute; Estados Unidos.Fil: Campbell, David A. University of California. Department of Microbiology; Estados Unidos.Fil: Carrington, Mark. University of Cambridge. Department of Biochemistry; Reino Unido.Fil: Crabtree, Jonathan. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Darban, Hamid. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Silveira, Jose Franco da. Universidade Federal de Sao Paulo. Departamento de Microbiologia; Brasil.Fil: Jong, Pieter de. Children’s Hospital Oakland Research Institute. BACPAC Resources; Estados Unidos.Fil: Edwards, Kimberly. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Englund, Paul T. Johns Hopkins University School of Medicine. Department of Biological Chemistry; Estados Unidos.Fil: Fazelina, Gholam. Seattle Biomedical Research Institute; Estados Unidos.Fil: Feldblyum, Tamara. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Ferella, Marcela. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Frasch, Alberto Carlos. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina.Fil: Gull, Keith. University of Oxford. Sir William Dunn School of Pathology; Reino Unido.Fil: Horn, David. London School of Hygiene and Tropical Medicine; Reino Unido.Fil: Hou, Lihua. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Huang, Yiting. Seattle Biomedical Research Institute; Estados Unidos.Fil: Kindlund, Ellen. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Klingbeil, Michele. University of Massachusetts. Department of Microbiology; Estados Unidos.Fil: Kluge, Sindy. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Koo, Hean. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Lacerda, Daniela. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Levin, Mariano J. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET-CYTED project). Laboratorio de Biología Molecular de la Enfermedad de Chagas; Argentina.Fil: Lorenzi, Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET-CYTED project). Laboratorio de Biología Molecular de la Enfermedad de Chagas; Argentina.Fil: Louie, Tin. Seattle Biomedical Research Institute; Estados Unidos.Fil: Machado, Carlos Renato. Universidade Federal de Minas Gerais. Departamento de Bioquímica e Imunologia; Brasil.Fil: McCulloch, Richard. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: McKenna, Alan. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Mizuno, Yumi. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Mottram, Jeremy C. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: Nelson, Siri. Seattle Biomedical Research Institute; Estados Unidos.Fil: Ochaya, Stephen. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Osoegawa, Kazutoyo. Children’s Hospital Oakland Research Institute. BACPAC Resources; Estados Unidos.Fil: Pai, Grace. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Parsons, Marilyn. Seattle Biomedical Research Institute; Estados Unidos.Fil: Pentony, Martin. Seattle Biomedical Research Institute; Estados Unidos.Fil: Pettersson, Ulf. Uppsala University. Department of Genetics and Pathology; Suecia.Fil: Pop, Mihai. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Ramirez, Jose Luis. Universidad Central de Venezuela. Instituto de Biología Experimental; Venezuela.Fil: Rinta, Joel. Seattle Biomedical Research Institute; Estados Unidos.Fil: Robertson, Laura. Seattle Biomedical Research Institute; Estados Unidos.Fil: Salzberg, Steven L. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Sanchez, Daniel O. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina.Fil: Seyler, Amber. Seattle Biomedical Research Institute; Estados Unidos.Fil: Sharma, Reuben. University of Cambridge. Department of Biochemistry; Reino Unido.Fil: Shetty, Jyoti. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Simpson, Anjana J. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Sisk, Ellen. Seattle Biomedical Research Institute; Estados Unidos.Fil: Tammi, Martti T. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Tarleton, Rick. University of Georgia. Center for Tropical and Emerging Global Diseases; Estados Unidos.Fil: Teixeira, Santuza. Universidade Federal de Minas Gerais. Departamento de Bioquímica e Imunologia; Brasil.Fil: Aken, Susan Van. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Vogt, Christy. Seattle Biomedical Research Institute; Estados Unidos.Fil: Ward, Pauline N. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: Wickstead, Bill. University of Oxford. Sir William Dunn School of Pathology; Reino Unido.Fil: Wortman, Jennifer. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: White, Owen. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Fraser, Claire M. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Stuart, Kenneth D. Seattle Biomedical Research Institute; Estados Unidos.Fil: Andersson, Björn. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Whole-genome sequencing of the protozoan pathogen Trypanosoma cruzi revealed that the diploid genome contains a predicted 22,570 proteins encoded by genes, of which 12,570 represent allelic pairs. Over 50% of the genome consists of repeated sequences, such as retrotransposons and genes for large families of surface molecules, which include trans-sialidases, mucins, gp63s, and a large novel family (>1300 copies) of mucin-associated surface protein (MASP) genes. Analyses of the T. cruzi, T. brucei, and Leishmania major (Tritryp) genomes imply differences from other eukaryotes in DNA repair and initiation of replication and reflect their unusual mitochondrial DNA. Although the Tritryp lack several classes of signaling molecules, their kinomes contain a large and diverse set of protein kinases and phosphatases; their size and diversity imply previously unknown interactions and regulatory processes, which may be targets for intervention

The genome sequence of Trypanosoma cruzi, etiologic agent of Chagas disease

Fil: El-Sayed, Najib M. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Myler, Peter J. Seattle Biomedical Research Institute; Estados Unidos.Fil: Bartholomeu, Daniella C. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Nilsson, Daniel. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Aggarwal, Gautam. Seattle Biomedical Research Institute; Estados Unidos.Fil: Tran, Anh-Nhi. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Ghedin, Elodie. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Worthey, Elizabeth A. Seattle Biomedical Research Institute; Estados Unidos.Fil: Delcher, Arthur L. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Blandin, Gaëlle. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Westenberger, Scott J. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Caler, Elisabet. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Cerqueira, Gustavo C. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Haas, Carole Branched Brian. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Anupama, Atashi. Seattle Biomedical Research Institute; Estados Unidos.Fil: Arner, Erik. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Åslund, Lena. Uppsala University. Department of Genetics and Pathology; Suecia.Fil: Attipoe, Philip. Seattle Biomedical Research Institute; Estados Unidos.Fil: Bontempi, Esteban. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Bringaud, Frédéric. Université Victor Segalen Bordeaux II. Laboratoire de Génomique Fonctionnelle des Trypanosomatides; Francia.Fil: Burton, Peter. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: Cadag, Eithon. Seattle Biomedical Research Institute; Estados Unidos.Fil: Campbell, David A. University of California. Department of Microbiology; Estados Unidos.Fil: Carrington, Mark. University of Cambridge. Department of Biochemistry; Reino Unido.Fil: Crabtree, Jonathan. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Darban, Hamid. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Silveira, Jose Franco da. Universidade Federal de Sao Paulo. Departamento de Microbiologia; Brasil.Fil: Jong, Pieter de. Children’s Hospital Oakland Research Institute. BACPAC Resources; Estados Unidos.Fil: Edwards, Kimberly. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Englund, Paul T. Johns Hopkins University School of Medicine. Department of Biological Chemistry; Estados Unidos.Fil: Fazelina, Gholam. Seattle Biomedical Research Institute; Estados Unidos.Fil: Feldblyum, Tamara. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Ferella, Marcela. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Frasch, Alberto Carlos. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina.Fil: Gull, Keith. University of Oxford. Sir William Dunn School of Pathology; Reino Unido.Fil: Horn, David. London School of Hygiene and Tropical Medicine; Reino Unido.Fil: Hou, Lihua. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Huang, Yiting. Seattle Biomedical Research Institute; Estados Unidos.Fil: Kindlund, Ellen. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Klingbeil, Michele. University of Massachusetts. Department of Microbiology; Estados Unidos.Fil: Kluge, Sindy. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Koo, Hean. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Lacerda, Daniela. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Levin, Mariano J. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET-CYTED project). Laboratorio de Biología Molecular de la Enfermedad de Chagas; Argentina.Fil: Lorenzi, Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET-CYTED project). Laboratorio de Biología Molecular de la Enfermedad de Chagas; Argentina.Fil: Louie, Tin. Seattle Biomedical Research Institute; Estados Unidos.Fil: Machado, Carlos Renato. Universidade Federal de Minas Gerais. Departamento de Bioquímica e Imunologia; Brasil.Fil: McCulloch, Richard. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: McKenna, Alan. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Mizuno, Yumi. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Mottram, Jeremy C. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: Nelson, Siri. Seattle Biomedical Research Institute; Estados Unidos.Fil: Ochaya, Stephen. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Osoegawa, Kazutoyo. Children’s Hospital Oakland Research Institute. BACPAC Resources; Estados Unidos.Fil: Pai, Grace. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Parsons, Marilyn. Seattle Biomedical Research Institute; Estados Unidos.Fil: Pentony, Martin. Seattle Biomedical Research Institute; Estados Unidos.Fil: Pettersson, Ulf. Uppsala University. Department of Genetics and Pathology; Suecia.Fil: Pop, Mihai. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Ramirez, Jose Luis. Universidad Central de Venezuela. Instituto de Biología Experimental; Venezuela.Fil: Rinta, Joel. Seattle Biomedical Research Institute; Estados Unidos.Fil: Robertson, Laura. Seattle Biomedical Research Institute; Estados Unidos.Fil: Salzberg, Steven L. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Sanchez, Daniel O. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina.Fil: Seyler, Amber. Seattle Biomedical Research Institute; Estados Unidos.Fil: Sharma, Reuben. University of Cambridge. Department of Biochemistry; Reino Unido.Fil: Shetty, Jyoti. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Simpson, Anjana J. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Sisk, Ellen. Seattle Biomedical Research Institute; Estados Unidos.Fil: Tammi, Martti T. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Fil: Tarleton, Rick. University of Georgia. Center for Tropical and Emerging Global Diseases; Estados Unidos.Fil: Teixeira, Santuza. Universidade Federal de Minas Gerais. Departamento de Bioquímica e Imunologia; Brasil.Fil: Aken, Susan Van. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Vogt, Christy. Seattle Biomedical Research Institute; Estados Unidos.Fil: Ward, Pauline N. University of Glasgow. Wellcome Centre for Molecular Parasitology; Reino Unido.Fil: Wickstead, Bill. University of Oxford. Sir William Dunn School of Pathology; Reino Unido.Fil: Wortman, Jennifer. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: White, Owen. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Fraser, Claire M. The Institute for Genomic Research. Department of Parasite Genomics; Estados Unidos.Fil: Stuart, Kenneth D. Seattle Biomedical Research Institute; Estados Unidos.Fil: Andersson, Björn. Karolinska Institutet. Center for Genomics and Bioinformatics; Suecia.Whole-genome sequencing of the protozoan pathogen Trypanosoma cruzi revealed that the diploid genome contains a predicted 22,570 proteins encoded by genes, of which 12,570 represent allelic pairs. Over 50% of the genome consists of repeated sequences, such as retrotransposons and genes for large families of surface molecules, which include trans-sialidases, mucins, gp63s, and a large novel family (>1300 copies) of mucin-associated surface protein (MASP) genes. Analyses of the T. cruzi, T. brucei, and Leishmania major (Tritryp) genomes imply differences from other eukaryotes in DNA repair and initiation of replication and reflect their unusual mitochondrial DNA. Although the Tritryp lack several classes of signaling molecules, their kinomes contain a large and diverse set of protein kinases and phosphatases; their size and diversity imply previously unknown interactions and regulatory processes, which may be targets for intervention

Outcome of acute hypoxaemic respiratory failure: insights from the LUNG SAFE Study

Background: Current incidence and outcome of patients with acute hypoxaemic respiratory failure requiring mechanical ventilation in the intensive care unit (ICU) are unknown, especially for patients not meeting criteria for acute respiratory distress syndrome (ARDS). Methods: An international, multicentre, prospective cohort study of patients presenting with hypoxaemia early in the course of mechanical ventilation, conducted during four consecutive weeks in the winter of 2014 in 459 ICUs from 50 countries (LUNG SAFE). Patients were enrolled with arterial oxygen tension/inspiratory oxygen fraction ratio ≤300 mmHg, new pulmonary infiltrates and need for mechanical ventilation with a positive end-expiratory pressure of ≥5 cmH2O. ICU prevalence, causes of hypoxaemia, hospital survival and factors associated with hospital mortality were measured. Patients with unilateral versus bilateral opacities were compared. Findings: 12 906 critically ill patients received mechanical ventilation and 34.9% with hypoxaemia and new infiltrates were enrolled, separated into ARDS (69.0%), unilateral infiltrate (22.7%) and congestive heart failure (CHF; 8.2%). The global hospital mortality was 38.6%. CHF patients had a mortality comparable to ARDS (44.1% versus 40.4%). Patients with unilateral-infiltrate had lower unadjusted mortality, but similar adjusted mortality compared to those with ARDS. The number of quadrants on chest imaging was associated with an increased risk of death. There was no difference in mortality comparing patients with unilateral-infiltrate and ARDS with only two quadrants involved. Interpretation: More than one-third of patients receiving mechanical ventilation have hypoxaemia and new infiltrates with a hospital mortality of 38.6%. Survival is dependent on the degree of pulmonary involvement whether or not ARDS criteria are reached

Mechanical ventilation in patients with cardiogenic pulmonary edema: a sub-analysis of the LUNG SAFE study

Background: Patients with acute respiratory failure caused by cardiogenic pulmonary edema (CPE) may require mechanical ventilation that can cause further lung damage. Our aim was to determine the impact of ventilatory settings on CPE mortality. Methods: Patients from the LUNG SAFE cohort, a multicenter prospective cohort study of patients undergoing mechanical ventilation, were studied. Relationships between ventilatory parameters and outcomes (ICU discharge/hospital mortality) were assessed using latent mixture analysis and a marginal structural model. Results: From 4499 patients, 391 meeting CPE criteria (median age 70 [interquartile range 59-78], 40% female) were included. ICU and hospital mortality were 34% and 40%, respectively. ICU survivors were younger (67 [57-77] vs 74 [64-80] years, p &lt; 0.001) and had lower driving (12 [8-16] vs 15 [11-17] cmH2O, p &lt; 0.001), plateau (20 [15-23] vs 22 [19-26] cmH2O, p &lt; 0.001) and peak (21 [17-27] vs 26 [20-32] cmH2O, p &lt; 0.001) pressures. Latent mixture analysis of patients receiving invasive mechanical ventilation on ICU day 1 revealed a subgroup ventilated with high pressures with lower probability of being discharged alive from the ICU (hazard ratio [HR] 0.79 [95% confidence interval 0.60-1.05], p = 0.103) and increased hospital mortality (HR 1.65 [1.16-2.36], p = 0.005). In a marginal structural model, driving pressures in the first week (HR 1.12 [1.06-1.18], p &lt; 0.001) and tidal volume after day 7 (HR 0.69 [0.52-0.93], p = 0.015) were related to survival. Conclusions: Higher airway pressures in invasively ventilated patients with CPE are related to mortality. These patients may be exposed to an increased risk of ventilator-induced lung injury. Trial registration Clinicaltrials.gov NCT02010073