Rol de enfermería en la aparición de infecciones asociadas a catéteres en pacientes hemodializados en UTI y posibles factores causales

El cateterismo venoso central es una opción confiable en situaciones clínicas que requieren inmediato acceso a la circulación, como lo es en el caso de los pacientes con uremia que necesitan del tratamiento de hemodiálisis. Se considera que las infecciones nosocomiales, son aquellas que se desarrollan después de 24 horas de estadía en la Unidad de Terapia Intensiva hasta 48 horas después de haber salido el paciente de esta unidad. Entre los microorganismos responsables de la infección de los catéteres en pacientes en hemodiálisis, el S. Aureus es el más importante. Por lo tanto, la prevención de infecciones asociadas a catéteres, debe ser considerada una prioridad en los programas de control de infecciones y de evaluación del control de calidad hospitalaria.Las infecciones de los accesos vasculares, son una importante causa de mortalidad y morbilidad en los pacientes en hemodiálisis. Aun así, el riesgo varía sustancialmente entre los distintos tipos de acceso que empleen en su uso, lo que permite establecer una línea ascendente de riesgo, posicionándose el catéter transitorio como el acceso de más alto riesgo. Este estudio está enfocado principalmente en la calidad de atención de enfermería y los posibles factores causales, los cuales pueden ser: el sitio de inserción, seguido de la colonización durante la inserción del catéter, la colonización del catéter por vía hematógena proveniente de otro foco infeccioso, la falta de técnica aséptica, y contaminación por iatrogenia, durante las excesivas manipulaciones del catéter, contaminación a través de las manos y tracto respiratorio del personal de salud. Además de esto, los pacientes en hemodiálisis son conocidos por ser inmunosuprimidos, atribuido mayoritariamente a enfermedades de base como lo son el lupus eritematoso sistémico (LES), la hipertensión arterial (HTA), diabetes mellitus tipo II (DM II), entre otras, además de la mala nutrición asociada particularmente a la uremia y tratamiento de hemodiálisis. Este trabajo de investigación tiene como objetivo determinar cuál es el rol de enfermería en la aparición de infecciones asociadas a catéteres en pacientes hemodializados y cuáles sus posibles causas en la Unidad de Terapia Intensiva en el 4º trimestre del año 2011 en el Hospital Central de MendozaFil: Leyva, Myriam. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Escuela de Enfermería..Fil: Pavet, Mariela. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Escuela de Enfermería..Fil: Salas, Verónica. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Escuela de Enfermería.

Plasminogen activator urokinase expression reveals TRAIL responsiveness and supports fractional survival of cancer cells

Peer reviewe

The role of DNA (de)methylation in immune responsiveness of Arabidopsis.

DNA methylation is antagonistically controlled by DNA-methyltransferases and DNA-demethylases. The level of DNA methylation controls plant gene expression on a global level. We have examined impacts of global changes in DNA methylation on the Arabidopsis immune system. A range of hypo-methylated mutants displayed enhanced resistance to the biotrophic pathogen Hyaloperonospora arabidopsidis (Hpa), whereas two hyper-methylated mutants were more susceptible to this pathogen. Subsequent characterization of the hypo-methylated nrpe1 mutant, which is impaired in RNA-directed DNA methylation, and the hyper-methylated ros1 mutant, which is affected in DNA demethylation, revealed that their opposite resistance phenotypes are associated with changes in cell wall defence and salicylic acid (SA)-dependent gene expression. Against infection by the necrotrophic pathogen Plectosphaerella cucumerina, nrpe1 showed enhanced susceptibility, which was associated with repressed sensitivity of jasmonic acid (JA)-inducible gene expression. Conversely, ros1 displayed enhanced resistance to necrotrophic pathogens, which was not associated with increased responsiveness of JA-inducible gene expression. Although nrpe1 and ros1 were unaffected in systemic acquired resistance to Hpa, they failed to develop transgenerational acquired resistance against this pathogen. Global transcriptome analysis of nrpe1 and ros1 at multiple time-points after Hpa infection revealed that 49% of the pathogenesis-related transcriptome is influenced by NRPE1- and ROS1-controlled DNA methylation. Of the 166 defence-related genes displaying augmented induction in nrpe1 and repressed induction in ros1, only 25 genes were associated with a nearby transposable element and NRPE1- and/or ROS1-controlled DNA methylation. Accordingly, we propose that the majority of NRPE1- and ROS1-dependent defence genes are regulated in trans by DNA methylation. This article is protected by copyright. All rights reserved

Ascorbate-mediated regulation of growth, photoprotection, and photoinhibition in Arabidopsis thaliana.

The requirements for ascorbate for growth and photosynthesis were assessed under low (LL; 250 µmol m-2 s-1) or high (HL; 1600 µmol m-2 s-1) irradiance in wild-type Arabidopsis thaliana and two ascorbate synthesis mutants (vtc2-1 and vtc2-4) that have 30% wild-type ascorbate levels. The low ascorbate mutants had the same numbers of leaves but lower rosette area and biomass than the wild type under LL. Wild-type plants experiencing HL had higher leaf ascorbate, anthocyanin, and xanthophyll pigments than under LL. In contrast, leaf ascorbate levels were not increased under HL in the mutant lines. While the degree of oxidation measured using an in vivo redox reporter in the nuclei and cytosol of the leaf epidermal and stomatal cells was similar under both irradiances in all lines, anthocyanin levels were significantly lower in the low ascorbate mutants than in the wild type under HL. Differences in the photosynthetic responses of vtc2-1 and vtc2-4 mutants were observed. Unlike vtc2-1, the vtc2-4 mutants had wild-type zeaxanthin contents. While both low ascorbate mutants had lower levels of non-photochemical quenching of chlorophyll a fluorescence (NPQ) than the wild type under HL, qPd values were greater only in vtc2-1 leaves. Ascorbate is therefore essential for growth but not for photoprotection

Low antioxidant concentrations impact on multiple signalling pathways in Arabidopsis thaliana partly through NPR1

Production of reactive oxygen species (ROS) is linked to signalling in both developmental and stress responses. The level of ROS is controlled by both production and removal through various scavengers including ascorbic acid and glutathione. Here, the role of low ascorbic acid or glutathione concentrations was investigated on ozone-induced cell death, defence signalling, and developmental responses. Low ascorbic acid concentrations in vtc1 activated expression of salicylic acid (SA)-regulated genes, a response found to be dependent on the redox-regulated transcriptional co-regulator NPR1. In contrast, low glutathione concentrations in cad2 or pad2 reduced expression of SA-regulated genes. Testing different responses to jasmonic acid (JA) revealed the presence of at least two separate JA signalling pathways. Treatment of the vtc1 mutant with JA led to hyper-induction of MONODEHYDROASCORBATE REDUCTASE3, indicating that low ascorbic acid concentrations prime the response to JA. Furthermore, NPR1 was found to be a positive regulator of JA-induced expression of MDHAR3 and TAT3. The vtc1 and npr1 mutants were sensitive to glucose inhibition of seed germination; an opposite response was found in cad2 and pad2. Overall, low ascorbic acid concentrations mostly led to opposite phenotypes to low glutathione concentrations, and both antioxidants interacted with SA and JA signalling pathways

TRAIL death receptors DR4 and DR5 mediate cerebral microvascular endothelial cell apoptosis induced by oligomeric Alzheimer's Aβ

Vascular deposition of amyloid-β (Aβ) in sporadic and familial Alzheimer's disease, through poorly understood molecular mechanisms, leads to focal ischemia, alterations in cerebral blood flow, and cerebral micro-/macro-hemorrhages, significantly contributing to cognitive impairment. Here, we show that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptors DR4 and DR5 specifically mediate oligomeric Aβ induction of extrinsic apoptotic pathways in human microvascular cerebral endothelial cells with activation of both caspase-8 and caspase-9. The caspase-8 inhibitor cellular FLICE-like inhibitory protein (cFLIP) is downregulated, and mitochondrial paths are engaged through BH3-interacting domain death agonist (Bid) cleavage. Upregulation of DR4 and DR5 and colocalization with Aβ at the cell membrane suggests their involvement as initiators of the apoptotic machinery. Direct binding assays using receptor chimeras confirm the specific interaction of oligomeric Aβ with DR4 and DR5 whereas apoptosis protection achieved through RNA silencing of both receptors highlights their active role in downstream apoptotic pathways unveiling new targets for therapeutic intervention

N-glycosylation of mouse TRAIL-R and human TRAIL-R1 enhances TRAIL-induced death.

APO2L/TRAIL (TNF-related apoptosis-inducing ligand) induces death of tumor cells through two agonist receptors, TRAIL-R1 and TRAIL-R2. We demonstrate here that N-linked glycosylation (N-glyc) plays also an important regulatory role for TRAIL-R1-mediated and mouse TRAIL receptor (mTRAIL-R)-mediated apoptosis, but not for TRAIL-R2, which is devoid of N-glycans. Cells expressing N-glyc-defective mutants of TRAIL-R1 and mouse TRAIL-R were less sensitive to TRAIL than their wild-type counterparts. Defective apoptotic signaling by N-glyc-deficient TRAIL receptors was associated with lower TRAIL receptor aggregation and reduced DISC formation, but not with reduced TRAIL-binding affinity. Our results also indicate that TRAIL receptor N-glyc impacts immune evasion strategies. The cytomegalovirus (CMV) UL141 protein, which restricts cell-surface expression of human TRAIL death receptors, binds with significant higher affinity TRAIL-R1 lacking N-glyc, suggesting that this sugar modification may have evolved as a counterstrategy to prevent receptor inhibition by UL141. Altogether our findings demonstrate that N-glyc of TRAIL-R1 promotes TRAIL signaling and restricts virus-mediated inhibition

The Tnt1 Retrotransposon Escapes Silencing in Tobacco, Its Natural Host

Retrotransposons' high capacity for mutagenesis is a threat that genomes need to control tightly. Transcriptional gene silencing is a general and highly effective control of retrotransposon expression. Yet, some retrotransposons manage to transpose and proliferate in plant genomes, suggesting that, as shown for plant viruses, retrotransposons can escape silencing. However no evidence of retrotransposon silencing escape has been reported. Here we analyze the silencing control of the tobacco Tnt1 retrotransposon and report that even though constructs driven by the Tnt1 promoter become silenced when stably integrated in tobacco, the endogenous Tnt1 elements remain active. Silencing of Tnt1-containing transgenes correlates with high DNA methylation and the inability to incorporate H2A.Z into their promoters, whereas the endogenous Tnt1 elements remain partially methylated at asymmetrical positions and incorporate H2A.Z upon induction. Our results show that the promoter of Tnt1 is a target of silencing in tobacco, but also that endogenous Tnt1 elements can escape this control and be expressed in their natural host

The Progeny of Arabidopsis thaliana Plants Exposed to Salt Exhibit Changes in DNA Methylation, Histone Modifications and Gene Expression

Plants are able to acclimate to new growth conditions on a relatively short time-scale. Recently, we showed that the progeny of plants exposed to various abiotic stresses exhibited changes in genome stability, methylation patterns and stress tolerance. Here, we performed a more detailed analysis of methylation patterns in the progeny of Arabidopsis thaliana (Arabidopsis) plants exposed to 25 and 75 mM sodium chloride. We found that the majority of gene promoters exhibiting changes in methylation were hypermethylated, and this group was overrepresented by regulators of the chromatin structure. The analysis of DNA methylation at gene bodies showed that hypermethylation in the progeny of stressed plants was primarily due to changes in the 5′ and 3′ ends as well as in exons rather than introns. All but one hypermethylated gene tested had lower gene expression. The analysis of histone modifications in the promoters and coding sequences showed that hypermethylation and lower gene expression correlated with the enrichment of H3K9me2 and depletion of H3K9ac histones. Thus, our work demonstrated a high degree of correlation between changes in DNA methylation, histone modifications and gene expression in the progeny of salt-stressed plants