Diseño y validación de un instrumento para el registro de reacciones adversas a la donación de sangre y sus componentes / Design and validation of a program for the registration of adverse reactions to blood donation and its components", "_i": "

Introducción: La donación de sangre y sus componentes es un procedimiento en el que intervienen elementos internos y externos, los que al interactuar pueden convertirse en factores determinantes para desencadenar una reacción adversa durante la donación; ésta se entiende como un evento inesperado que pone en riesgo la salud del donante. Objetivo: Diseñar y validar un instrumento para registrar las reacciones adversas durante la donación de sangre y sus componentes que apoye la práctica de la enfermería de manera sistemática y ordenada. Material y métodosEstudio no experimental, transversal y prospectivo, en el que se diseñó un instrumento para el registro de reacción adversa durante la donación. Se validó por opinión de expertos de diferentes bancos de sangre de instituciones públicas en el período del 01 de enero al 31 de diciembre de 2011. Para determinar la consistencia interna, se utilizó la prueba de alfa de Cronbach con datos de 60 donantes que presentaron reacción adversa durante la donación durante o después del proceso de extracción de sangre. Resultados: El instrumento diseñado se integra de acuerdo con lo revisado en la literatura y con las observaciones y sugerencias aportadas por los expertos. Para procesar los datos se utilizó el programa SPSS versión 2.0; para calcular la confiabilidad del instrumento se determinó la consistencia del alfa de Cronbach, la cual arrojó un coeficiente de confiabilidad de α = 0.915 con 134 elementos analizados. Conclusiones: Se logra la validación y se cumple el objetivo de contar con un instrumento que permite el registro de reacción adversa durante la donación, apoyando el actuar de enfermería de manera ordenada y sistemática.

Introduction: The donation of blood and blood components is a procedure that involves internal an external elements which may become by interacting, determinans to trigger an adverse reaction during the donation; this is understood to be an unexpected event that threatens donor health. Objective: To design and validate and instrument to record adverse reactions to blood and its components donation in a systematic an orderly way to support nursing practice. Material and methods: Non-experimental, cross-sectional and prospective study in which and instrument was designed to record adverse reactions to donation. The instrument was validate by experts from different public blood banks in the period from January 1 to December 31, 2011. To determine the internal consistency, we used Cronbach’s alpha test with data from 60 donors who present adverse reaction during or after blood extraction procedure. Results: The designed instrument was integrated according to the reviewed literature and the comments and suggestions made be experts. To process the data, we used SPSS software version 2.0; to calculate the reliability of the instrument, we determined the consistency of Cronbach’s alpha, which yielded reliability coefficient of α = 0.915 with 134 elements analyzed. Conclusions: The validation is achieved and meets the objective of having an instrument that enables the recording of adverse reaction to blood and its components donation, thus supporting nursing performance in a systematic and orderly way.

PCB uptake and accumulation by oysters (Crassostrea virginica) exposed via a contaminated algal diet.

Reproductively active oysters were fed daily with 0.2 g algal paste containing 0, 0.1, and 1.0 microgram polychlorinated biphenyls (PCBs) (1:1:1 mixture of Aroclor 1242, 1254 and 1260) for either 15 or 30 days, and accumulation of PCBs in different organ tissues and eggs assessed. The effects of PCB exposure on lipid content, lipid class and fatty acid composition were also evaluated. PCBs were accumulated by the oysters and transferred to the eggs. PCB accumulation in oysters was dose, time and tissue dependent. Mean PCB contents were 3150, 1970, and 250 ng/g dry wt., respectively, in the visceral mass, gills + mantle and muscle of oysters fed algal paste containing 1.0 microgram PCBs for 30 days. The PCBs in the eggs from the same oysters reached 671 ng PCBs/g dry wt. Feeding oysters with PCB-sorbed algal paste for 30 days significantly increased phospholipid and free fatty acid contents in gills + mantle tissue compared to the same tissues in the undosed control.

Effects of PCBs sorbed to algal paste and sediments on the stress protein response (HSP70 family) in the eastern oyster, Crassostrea virginica.

This study examined the stress protein response (HSP70 family) of reproductively inactive oysters fed 0.7 g algal paste containing 0, 0.35 and 3.5 micrograms polychlorinated biphenyls (PCBs) daily. A second set of treatment groups investigated the combined effect of PCBs and sediments (0.3 g sediments daily per oyster) on HSP70 response. After 8 weeks of PCB exposure, oyster tissues (mantle and gill) were sampled and analyzed for HSP70. Preliminary results did not show a significant effect in HSP70 response in oysters fed PCB sorbed to algal paste, albeit PCBs accumulated up to 1342 ng/g dry weight in the mantle, and up to 180 ng/g dry weight in gill tissues. However, the addition of sediments caused a significant increase in HSP70 levels of gills and mantle, although the mantle was less sensitive to the sediments.

Membrane-associated redox cycling of copper mediates hydroperoxide toxicity in Escherichia coli.

We are studying the action of tert-butylhydroperoxide (t-BOOH) on Escherichia coli as a model system for peroxide toxicity. In our previous report (De la Cruz-Rodriguez, L.C., Farías, R.N. and Massa, E.M. (1990) Biochim. Biophys. Acta 1015, 510-516), the respiratory chain was identified as a major target of t-BOOH. In the present paper, we study further the effect of t-BOOH on the NADH oxidase of the E. coli respiratory chain to clarify the mechanism of damage, especially regarding the identity and role of the metal ion involved. The results are: (a) t-BOOH toxicity is mediated by membrane-bound copper ions; (b) a small pool of the membrane-bound copper is reduced from Cu(II) to Cu(I) in the presence of NADH and other respiratory substrates (succinate, D-lactate); (c) this reduction of copper occurs at 37 degrees C but not at 0 degrees C or when the membranes are inactivated by previous heating; (d) the Cu(I) generated by reduction of Cu(II) during membrane preincubation with NADH, is oxidized by t-BOOH with simultaneous inactivation of the NADH oxidase, whereas treatment with only t-BOOH (without NADH) has no effect on the oxidase. It is concluded that the effect of t-BOOH on the respiratory chain is mediated by redox cycling of copper. It is proposed that the damage results from activation of the hydroperoxide through its interaction with Cu(I) in a site-specific Fenton-type reaction.

Damage of Escherichia coli cells by t-butylhydroperoxide involves the respiratory chain but is independent of the presence of oxygen.

The action of t-butylhydroperoxide (tBOOH) on Escherichia coli cells has been studied as a model system for organic peroxide toxicity. Exposure of E. coli cells to tBOOH led to progressive and irreversible impairment of the respiratory function, an effect which was dependent on the availability of substrate. The effect of tBOOH on growth of E. coli with different carbon sources and alternative terminal electron acceptors was investigated. It was found that the sensitivity of E. coli to tBOOH under diverse growth conditions implicating a functional respiratory chain was greater than when the bacterium grew by fermentation. Also the mutant E. coli SASX76, which requires exogenous 5-aminolevulinic acid to synthesize the cytochromes, was more resistant to tBOOH when lacking a functional respiratory chain. These data point to the respiratory chain as a major target in the in vivo action of tBOOH. Experiments with isolated membranes also showed a tBOOH-induced damage of the respiratory chain monitored by impairment of the NADH oxidase. The effect of tBOOH was produced even under anaerobiosis, indicating that development of cell damage was independent of oxygen and, therefore, that neither oxygen-derived radicals nor lipid peroxidation were involved.