Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU

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Paternal and maternal mutations in X-STRs: a GHEP-ISFG collaborative study

The GHEP-ISFG organized a collaborative study to estimate mutation rates for the markers included in the Investigator Argus X-12 QS kit Qiagen. A total of 16 laboratories gathered data from 1,612 father/mother/daughter trios, which were used to estimate both maternal and paternal mutation rates, when pooled together with other already published data. Data on fathers and mothers’ age at the time of birth of the daughter were also available for ∼93 % of the cases. Population analyses were computed considering the genetic information of a subset of 1,327 unrelated daughters, corresponding to 2,654 haplotypes from residents in several regions of five countries: Argentina, Brazil, Ecuador, Portugal and Spain. Genetic differentiation analyses between the population samples from the same country did not reveal signs of significant stratification, although results from Hardy-Weinberg and linkage disequilibrium tests indicated the need of larger studies for Ecuador and Brazilian populations. The high genetic diversity of the markers resulted in a large number of haplotype combinations, showing the need of huge databases for reliable estimates of their frequencies. It should also be noted the high number of new alleles found, many of them not included in the allelic ladders provided with the kit, as very diverse populations were analyzed. The overall estimates for locus specific average mutation rates varied between 7.5E-04 (for DXS7423) and 1.1E-02 (for DXS10135), the latter being a troublesome figure for kinship analyses. Most of the found mutations (∼92 %) are compatible with the gain or loss of a single repeat. Paternal mutation rates showed to be 5.2 times higher than maternal ones. We also found that older fathers were more prone to transmit mutated alleles, having this trend not been observed in the case of the mothers.Institute of Pathology and Molecular Immunology from University of Porto (IPATIMUP)Instituto de Investigação e Inovação em Saúde I3S Universidade do PortoCMUP Centro de Matemática da Universidade do PortoSection of Forensic Genetics Department of Forensic Medicine Faculty of Health and Medical Sciences University of CopenhagenLaboratório de Diagnóstico por DNA (LDD) Universidade do Estado do Rio de JaneiroCentro de Genética Forense Poder Judicial de CórdobaLaboratorio Regional de Investigación Forense Tribunal Superior de Justicia de Santa CruzUNESP-Universidade Estadual Paulista Faculdade de Ciências Farmacêuticas Laboratório de Investigação de Paternidade-NACInstituto Nacional de Medicina Legal e Ciências Forenses I.P. Serviço de Genética e Biologia Forenses Delegação do CentroEscuela de Medicina Facultad de Ciencias de la Salud Universidad de Las Américas (UDLA)Laboratorio de ADN de la Fiscalía General del EstadoDepartamento de Biología Servicio de Criminalística de la Guardia CivilLaboratorio Regional de Genética Forense Poder Judicial de Río NegroInstituto Nacional de Medicina Legal e Ciências Forenses I.P. Serviço de Genética e Biologia Forenses Delegação do NortePRICAI-Fundación FavaloroLaboratorio de Análisis de ADN Facultad de Ciencias Médicas Universidad Nacional de CuyoLabGenetics: Laboratorio de Genética Clínica S.L.Genomic Engenharia Molecular MolecularLaboratorio de Genética Forense Poder Judicial de la Provincia de La PampaLaboratorio MANLAB Área de FiliacionesUNESP-Universidade Estadual Paulista Faculdade de Ciências Farmacêuticas Laboratório de Investigação de Paternidade-NA

Kidney and Liver Injuries After Major Burns in Rats Are Prevented by Resolvin D2

BACKGROUND: Innate immune dysfunction after major burn injuries increases the susceptibility to organ failure. Lipid mediators of inflammation resolution, e.g. Resolvin D2 (RvD2), have been shown recently to restore neutrophil functionality and reduce mortality rate in a rat model of major burn injury. However, the physiological mechanisms responsible for the benefic activity of RvD2 are not well understood. DESIGN: Prospective randomized animal investigation. SETTING: Academic research setting. SUBJECTS: Wistar male rats. INTERVENTIONS: Animals were subjected to a full thickness skin burn of 30% total body surface area. Two hours after burn, 25 ng/kg RvD2 was administered i.v. and repeated every day, for 8 days. At day 10 post burn (pb), 2 mg/kg of lipopolysaccharide (LPS) was administered i.v., and the presence of renal and hepatic injuries was evaluated at day 11 pb by immunohistochemistry and relevant blood chemistry. MEASUREMENTS AND MAIN RESULTS: In untreated animals, we found significant tissue damage in the kidney and liver, consistent with acute tubular necrosis and multifocal necrosis, and changes in blood chemistry, reflecting the deterioration of renal and hepatic functions. In RvD2 treated rats, we detected less tissue damage and significantly lower values of blood urea nitrogen (BUN) (26.4±2.1 vs. 36.0±9.3 mg/dl, p≤0.001), alanine aminotransferase (ALT) (266.5±295.2 vs. 861.8±813.7 U/l, p≤0.01), and total bilirubin (0.13±0.05 vs. 0.30±0.14 mg/dl, p≤0.01), compared to untreated animals. The mean blood pressure of all animals was above 65 mmHg, indicating adequate tissue perfusion throughout the experiments. We measured significantly larger amounts of chromatin in the circulation of untreated compared to RvD2 treated rats (575.1±331.0 vs. 264.1±122.4 ng/ml, p≤0.05) and identified neutrophil extracellular traps (NETs) in kidney and liver tissues from untreated rats, consistent with the tissue damage. CONCLUSIONS: Pathological changes in kidney and liver tissues in a rat model of major burn and endotoxin insults are ameliorated by RvD2