Closed-loop control of renal perfusion pressure in physiological experiments.

This paper presents the design, experimental modeling, and control of a pump-driven renal perfusion pressure (RPP)-regulatory system to implement precise and relatively fast RPP regulation in rats. The mechatronic system is a simple, low-cost, and reliable device to automate the RPP regulation process based on flow-mediated occlusion. Hence, the regulated signal is the RPP measured in the left femoral artery of the rat, and the manipulated variable is the voltage applied to a dc motor that controls the occlusion of the aorta. The control system is implemented in a PC through the LabView software, and a data acquisition board NI USB-6210. A simple first-order linear system is proposed to approximate the dynamics in the experiment. The parameters of the model are chosen to minimize the error between the predicted and experimental output averaged from eight input/output datasets at different RPP operating conditions. A closed-loop servocontrol system based on a pole-placement PD controller plus dead-zone compensation was proposed for this purpose. First, the feedback structure was validated in simulation by considering parameter uncertainty, and constant and time-varying references. Several experimental tests were also conducted to validate in real time the closed-loop performance for stepwise and fast switching references, and the results show the effectiveness of the proposed automatic system to regulate the RPP in the rat, in a precise, accurate (mean error less than 2 mmHg) and relatively fast mode (10-15 s of response time).

[In vitro activities of colistin combinations against Pseudomonas aeruginosa isolated from the intensive care unit]. / Actividad in vitro de terapia combinada con colistina frente a Pseudomonas aeruginosa aisladas en Unidad de Cuidados Intensivos.

Introduction. As the number of multidrug-resistant strains of Pseudomonas aeruginosa has risen in the intensive care unit (ICU) of the San Carlos Clinic Hospital, 12 consecutive isolates from different patients were collected to determine the possibility of an epidemic outbreak caused by the spread of a single strain. We determined the antimicrobial susceptibility to the most common agents used in the treatment of infections caused by this bacteria. The results of susceptibility studies suggest that different strains of P. aeruginosa are responsible for the respiratory tract infections in ICU. Methods. The clonal relationship between the isolates using was determined using BOX and ERIC primers by means of repetitive sequence-based polymerase chain reaction (rep-PCR). The in vitro activity of these strains against colistin, rifampicin, doxicycline and azythromycin was studied to determine in which cases the combination of colistin with any of the other three antibiotics was synergistic. Results. Sensitivity studies point out the presence of several strains of P. aeruginosa as the causal agents of respiratory infections produced by this microorganism in the ICU. Combinations of colistin with doxycicline and colistin with azithromycin were synergistic for some isolates in the synergy studies. Discussion. Clonal studies reveal the presence of five different clones among our isolates. Therefore we can conclude that there was no outbreak of P. aeruginosa in the ICU. Synergistic activity of combinations of colistin plus azithromycin, colistin plus doxicycline and colistin plus rifampicin was less than expected and a high percentage of indifferent results was observed.

Actividad in vitro de terapia combinada con colistina frente a Pseudomonas aeruginosa aisladas en Unidad de Cuidados Intensivos / In vitro activities of colistin combinations against Pseudomonas aeruginosa isolated from the intensive care unit

Introducción. Ante el incremento de aislados de Pseudomonasaeruginosa multirresistentes en la Unidad de CuidadosIntensivos (UCI) del Hospital Clínico San Carlos deMadrid y para determinar la posibilidad de que se tratase deun brote epidémico causado por la diseminación de unaúnica cepa, se recogieron 12 muestras consecutivas de distintospacientes que fueron identificadas y a las que posteriormentese determinó su sensibilidad a los antibióticosutilizados habitualmente para el tratamiento de las infeccionesproducidas por este microorganismo.Métodos. Mediante la amplificación de secuencia basadaen la reacción en cadena de la polimerasa (repetitive sequence-based polymerase chain reaction, rep-PCR) se determinó larelación clonal entre los aislados utilizando los primers BOX yERIC y se estudió la actividad in vitro frente a estas cepas decolistina, rifampicina, doxiciclina y azitromicina para determinaren qué casos la combinación de colistina con alguno de losotros tres antibióticos presentaba actividad sinérgica.Resultados. Los estudios de sensibilidad apuntan a la presenciade varias cepas de P. aeruginosa como responsables delas infecciones respiratorias producidas por este microorganismoen la UCI, hecho que fue corroborado mediante los estudiosclonales realizados. En los estudios de sinergia las asociacionesde colistina con doxiciclina y con azitromicina presentaron actividadsinérgica para alguno de los aislados.Discusión. Los resultados de los estudios clonales revelanla presencia de cinco clones diferentes entre los aisladosseleccionados, por lo que podemos concluir que no se tratade un brote de P. aeruginosa en la UCI. La actividad sinérgicade la asociación de colistina con azitromicina, doxiciclinay rifampicina ha sido menor de la esperada y se observa unelevado porcentaje de resultados indiferentes (AU)

Introduction. As the number of multidrug-resistantstrains of Pseudomonas aeruginosa has risen in the intensivecare unit (ICU) of the San Carlos Clinic Hospital,12 consecutive isolates from different patients were collectedto determine the possibility of an epidemic outbreakcaused by the spread of a single strain. We determinedthe antimicrobial susceptibility to the most commonagents used in the treatment of infections caused by thisbacteria. The results of susceptibility studies suggest thatdifferent strains of P. aeruginosa are responsible for therespiratory tract infections in ICU.Methods. The clonal relationship between the isolatesusing was determined using BOX and ERIC primersby means of repetitive sequence-based polymerase chainreaction (rep-PCR). The in vitro activity of these strainsagainst colistin, rifampicin, doxicycline and azythromycinwas studied to determine in which cases the combinationof colistin with any of the other three antibioticswas synergistic.Results. Sensitivity studies point out the presence ofseveral strains of P. aeruginosa as the causal agents ofrespiratory infections produced by this microorganism inthe ICU. Combinations of colistin with doxycicline andcolistin with azithromycin were synergistic for some isolatesin the synergy studies.Discussion. Clonal studies reveal the presence of fivedifferent clones among our isolates. Therefore we canconclude that there was no outbreak of P. aeruginosa inthe ICU. Synergistic activity of combinations of colistinplus azithromycin, colistin plus doxicycline and colistinplus rifampicin was less than expected and a high percentageof indifferent results was observed (AU)

The aberrant cell walls of boron-deficient bean root nodules have no covalently bound hydroxyproline-/proline-rich proteins.

B-deficient bean (Phaseolus vulgaris L.) nodules examined by light microscopy showed dramatic anatomical changes, mainly in the parenchyma region. Western analysis of total nodule extracts examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that one 116-kD polypeptide was recognized by antibodies raised against hydroxyproline-rich glycoproteins (HRGPs) from the soybean (Glycine max) seed coat. A protein with a comparable molecular mass of 116 kD was purified from the cell walls of soybean root nodules. The amino acid composition of this protein is similar to the early nodulin (ENOD2) gene. Immunoprecipitation of the soybean ENOD2 in vitro translation product showed that the soybean seed coat anti-HRGP antibodies recognized this early nodulin. Furthermore, we used these antibodies to localize the ENOD2 homolog in bean nodules. Immunocytochemistry revealed that in B-deficient nodules ENOD2 was absent in the walls of the nodule parenchyma. The absence of ENOD2 in B-deficient nodules was corroborated by performing hydroxyproline assays. Northern analysis showed that ENOD2 mRNA is present in B-deficient nodules; therefore, the accumulation of ENOD2 is not affected by B deficiency, but its assembly into the cell wall is. B-deficient nodules fix much less N2 than control nodules, probably because the nodule parenchyma is no longer an effective O2 barrier.