11 research outputs found

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

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    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

    Biological cycle of Argas (Persicargas) keiransi fed on hen´s blood under laboratory conditions

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    A. keiransi Estrada-Peria, Venzal & Gonzalez-Acufia (Acari: Argasidae) be-long to the subgenus Persicargas, which includes soft bodied ticks distributed worldwide and commonly found parasitizing birds (Klompen, 1992). Argas (Persicargas) keiransi was described from engorged larvae of the Chimango Caracara (Milvago chimango chimango Vieillot (Ayes: Falconiformes: Falconi-dae: Caracarinae)) from Chillan (Bio Bio Region), Chile (Estrada-Pena et al. 2003). Females of A. keiransi were later described by Estrada-Pefla et al. (2006), also based on specimens from Chillan. The objective of this study was to describe the biological cycle of A. keiransi under laboratory conditions and compare it with related species.Fil: Ardiles, Karen. Universidad de Concepcion del Uruguay; ArgentinaFil: González Acuña, D.. Universidad de Concepcion del Uruguay; ArgentinaFil: Sepulveda, Maria Soledad. Purdue University; Estados UnidosFil: Vargas, Pamela. Universidad de Concepción; ChileFil: Guglielmone, Alberto Alejandro. Instituto Nacional de Tecnologia Agropecuaria. Centro Regional Santa Fe. Estacion Experimental Agropecuaria Rafaela; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Santa Fe; Argentin

    AID overexpression leads to aggressive murine CLL and non-Ig mutations that mirror human neoplasms.

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    International audienceMost cancers become more dangerous by the outgrowth of malignant subclones with additional DNA mutations that favor proliferation or survival. Using chronic lymphocytic leukemia (CLL), a disease exemplary of this process, and a model for neoplasms in general, we created transgenic mice overexpressing the enzyme, activation-induced deaminase (AID), whose normal function is to induce DNA mutations in B lymphocytes. AID allows normal B lymphocytes to develop more effective immunoglobulin (Ig)-mediated immunity, but also is able to mutate non-Ig genes, predisposing to cancer. In chronic lymphocytic leukemia (CLL), AID expression correlates with poor prognosis suggesting a role for this enzyme in disease progression. Nevertheless, direct experimental evidence identifying the specific genes that are mutated by AID and indicating that those genes are associated with disease progression is not available. To address this point, we overexpressed Aicda in a murine model of CLL (Em-TCL1). Analyses of TCL1/AID mice demonstrate a role for AID in disease kinetics, CLL-cell proliferation, and the development of cancer-related target mutations with canonical AID signatures in non-Igs genes. Notably, our mouse models can accumulate mutations in the same genes that are mutated in human cancers. Moreover, some of these mutations occur at homologous positions, leading to identical or chemically-similar amino acid substitutions as in human CLL and lymphoma.Together, these findings support a direct link between aberrant AID activity and CLL driver mutations that are then selected for their oncogenic effects, whereby AID promotes aggressiveness in CLL and other B-cell neoplasms

    AID overexpression leads to aggressive murine CLL and non-Ig mutations that mirror human neoplasms.

    No full text
    Most cancers become more dangerous by the outgrowth of malignant subclones with additional DNA mutations that favor proliferation or survival. Using chronic lymphocytic leukemia (CLL), a disease exemplary of this process, and a model for neoplasms in general, we created transgenic mice overexpressing the enzyme, activation-induced deaminase (AID), whose normal function is to induce DNA mutations in B lymphocytes. AID allows normal B lymphocytes to develop more effective immunoglobulin (Ig)-mediated immunity, but also is able to mutate non-Ig genes, predisposing to cancer. In chronic lymphocytic leukemia (CLL), AID expression correlates with poor prognosis suggesting a role for this enzyme in disease progression. Nevertheless, direct experimental evidence identifying the specific genes that are mutated by AID and indicating that those genes are associated with disease progression is not available. To address this point, we overexpressed Aicda in a murine model of CLL (Em-TCL1). Analyses of TCL1/AID mice demonstrate a role for AID in disease kinetics, CLL-cell proliferation, and the development of cancer-related target mutations with canonical AID signatures in non-Igs genes. Notably, our mouse models can accumulate mutations in the same genes that are mutated in human cancers. Moreover, some of these mutations occur at homologous positions, leading to identical or chemically-similar amino acid substitutions as in human CLL and lymphoma.Together, these findings support a direct link between aberrant AID activity and CLL driver mutations that are then selected for their oncogenic effects, whereby AID promotes aggressiveness in CLL and other B-cell neoplasms.Fil: Morande, Pablo Elías. Instituto Pasteur de Montevideo; Uruguay. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Yan, Xiao Jie. The Feinstein Institute For Medical Research; Estados UnidosFil: Sepulveda Yanez, Julieta Haydee. Universidad de Magallanes; ChileFil: Seija, Noé. Instituto Pasteur de Montevideo; UruguayFil: Marquez, Maria Elena. Instituto Pasteur de Montevideo; UruguayFil: Sotelo, Natalia Soledad. Instituto Pasteur de Montevideo; UruguayFil: Abreu, Cecilia. Instituto Pasteur de Montevideo; UruguayFil: Crispo, Martina. Instituto Pasteur de Montevideo; UruguayFil: Fernández Graña, Gabriel. Instituto Pasteur de Montevideo; UruguayFil: Rego, Natalia. Instituto Pasteur de Montevideo; UruguayFil: Bois, Therence. Institut de Recherches Cliniques de Montréal; CanadáFil: Methot, Stephen Patrick. Institut de Recherches Cliniques de Montréal; CanadáFil: Palacios, Florencia. The Feinstein Institute For Medical Research; Estados UnidosFil: Remedi, Victoria. Hospital Maciel Montevideo; UruguayFil: Rai, Kanti R.. The Feinstein Institute For Medical Research; Estados UnidosFil: Buschiazzo, Alejandro. Instituto Pasteur de Montevideo; UruguayFil: Di Noia, Javier Marcelo. Institut de Recherches Cliniques de Montréal; CanadáFil: Navarrete, Marcelo Alejandro. Universidad de Magallanes; ChileFil: Chiorazzi, Nicholas. The Feinstein Institute For Medical Research; Estados UnidosFil: Oppezzo, Pablo. Instituto Pasteur de Montevideo; Urugua

    Empowering Latina scientists

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    Correction to: Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study (Intensive Care Medicine, (2021), 47, 2, (160-169), 10.1007/s00134-020-06234-9)

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    The original version of this article unfortunately contained a mistake. The members of the ESICM Trials Group Collaborators were not shown in the article but only in the ESM. The full list of collaborators is shown below. The original article has been corrected
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