Sorption and inhibitory effect of octylphenol ethoxylate Triton X-100 on methanogenic and denitrifying granular sludges.

The aims of this work were to characterize the sorption and evaluate the inhibitory effect of octylphenol ethoxylate Triton X-100 (OPEOTx) on methanogenic and denitrifying sludges. According to Langmuir isotherm, maximums OPEOTx sorption values on methanogenic and denitrifying sludges were 60.70 mg (gVSS)-1 and 87.47 mg (gVSS)-1 respectively. The specific removal rate of chemical oxygen demand (rCOD) and the accumulated volume biogas (VBG) were used to evaluate the OPEOTx inhibitory effect on sludges. Experimental inhibition data were fitted to the models of non-competitive inhibition and modified Gompertz. Methanogenic sludges reached higher levels inhibition in the rCOD and biogas production potential Pmax (84.0 and 88.5%) comparing with denitrifying sludges (24.3 and 21.9%). Furthermore, in all OPEOTx concentrations, carbohydrates-proteins quotient value of the extracellular polymeric substances for the denitrifying sludges remained below respect to the same quotient in methanogenic sludges. The above contributes in part to explain the greater sorption capacity of the denitrifying sludges by OPEOTx and their granules resistance to be damaged by OPEOTx amphiphilic nature. The study gives insights to understand OPEOs interactions and their effects on methanogenic and denitrifying granular sludges.

Modeling wastewater biodecolorization with reactive blue 4 in fixed bed bioreactor by Trametes subectypus: biokinetic, biosorption and transport.

A biodecolorization model that considers the simultaneous mechanism of biosorption and biodegradation of a synthetic dye by immobilized white-rot fungus Trametes subectypus B32 in a fixed bed bioreactor was developed. The model parameters (biokinetic, biosorption and macroscopic transport) were determined by independent experiments. The biodecolorization model was used to determine the effect of variables such as immobilized biomass content, volumetric flow of wastewater, dye feeding concentration and initial dye concentration. By means of the model was possible to predict in the steady state, the limits of immobilized T. subectypus to biodecolorize polluted influent, being the model predictions similar in extent to previous reports. A dimensionless module of biosorption-bioreaction (ϕ=q(max)v(z)/r(max)L) was proposed to be used like criterion whenever one of the two mechanisms controls the biodecolorization. The model could be used for the designing and scaling up of fixed bed bioreactors with immobilized white-rot fungi for the biodecolorization process.

[Severe sepsis as a cause of acute renal failure]. / Sepsis severa como causa de falla renal aguda.

INTRODUCTION: The most common causes of acute renal failure in the intensive care units are severe sepsis and septic shock. Mortality reported in this kind of patients is about 70%. The pathophysiology of acute renal failure in severe sepsis includes systemic hypotension, direct renal vasoconstriction, infiltration of the kidney by inflammatory cells, renal ischemia, intraglomerular thrombosis and intratubular obstruction. OBJECTIVE: To show the incidence, mortality and histopathological etiology of acute renal failure in severe sepsis. TYPE STUDY: Retrospective, transversal and descriptive. METHODS: We study 332 cases of patients with severe sepsis, who were hospitalized in the Intensive Care Unit of Hospital General del Centro Médico Nacional, during five years. From these patients 107 developed acute renal failure due to severe sepsis. This group recived two differet kind of treatment, medical management (70%) and hemodyalisis (30%). Renal biopsy was taken in 40 patients after six or seven days of the diagnosis of acute renal failure caused by severe sepsis. RESULTS: In the group of 332 patients with severe sepsis 107 developed acute renal failure, this represents the 32.22%. The group of patients with renal biopsy presented the following results: 50% had acute tubular necrosis, 27.5% presented glomerular and tubular lesion, the rest 22.5% had glomerular and vascular lesion. The mortality for patients treated with medical management was of 69.3%, and for those treated with hemodyalisis was of 28.1%. DISCUSSION: Nowadays, and due to the high incidence and mortality of this disease, is very important to generate more concise knowledge about the genesis and development of acute renal failure in the septic patient.

Sepsis severa como causa de falla renal aguda / Severe sepsis as a cause of acute renal failure

Introducción: Las causas más comunes de insuficiencia renal aguda en las unidadesde cuidados intensivos son la sepsis severa y el choque séptico. La mortalidadreportada en los pacientes con sepsis severa e IRA es hasta del 70%. Lafisiopatología propuesta para la falla renal en la sepsis grave incluye una combinaciónde factores como hipotensión sistémica, vasoconstricción renal, infiltraciónde células inflamatorias en el riñón, trombosis intraglomerular y obstrucción intratubular.Objetivos: Mostrar la incidencia, mortalidad y la histología de la insuficienciarenal aguda causada por sepsis severa.Diseño del estudio: Retrospectivo, descriptivo y transversal.Metodología: Se estudiaron retrospectivamente los casos de 332 pacientes conel diagnóstico de sepsis severa que fueron hospitalizados en la Unidad de CuidadosIntensivos del Hospital General del Centro Médico Nacional en el lapso deun lustro. De este total de pacientes 107 presentaron insuficiencia renal aguda secundariaa dicho proceso séptico. El diagnóstico se efectuó con base en las alteracionesde las pruebas funcionales renales (DCr, DmOms, DH20, U/PmOsm,FENA, FEK y IFR). Los pacientes fueron tratados de dos modos distintos, mediantemanejo médico (70%) o con hemodiálisis (30%). A 40 de ellos se les tomóbiopsia renal percutánea entre los seis y siete días posteriores a su diagnóstico.Todas las biopsias fueron estudiadas por microscopia óptica.Resultados: Del grupo de 332 pacientes con sepsis severa 107 presentó insuficienciarenal aguda, lo que representa el 32,22% de la población en este grupo40 pacientes (100%) a los que se les tomó biopsia renal; 20 pacientes (50%) tuvieronnecrosis tubulointersticial, 11 pacientes (27,5%) desarrollaron lesión glomerulary tubular, y el resto 9 pacientes (22,5%) presentaron lesión glomerular yvascular.La mortalidad para el grupo tratado con manejo médico fue del 69,3%, mientrasque la del grupo tratado con hemodiálisis fue del 28,1%.Discusión: Es necesario generar conocimientos más exactos sobre la génesis ydesarrollo de la IRA en el paciente séptico, ya que la mortalidad en estos pacientescontinua siendo elevada a pesar del inicio de diálisis temprana en cualquierade sus modalidades, aun con las de reemplazo renal continuo

Introduction: The most common causes of acute renal failure in the intensivecare units are severe sepsis and septic shock. Mortality reported in this kind ofpatients is about 70%. The pathophysiology of acute renal failure in severe sepsisincludes systemic hypotension, direct renal vasoconstriction, infiltration of thekidney by inflammatory cells, renal ischemia, intraglomerular thrombosis and intratubularobstruction.Objective: To show the incidence, mortality and histopathological etiology ofacute renal failure in severe sepsis.Type study: Retrospective, transversal and descriptive.Methods: We study 332 cases of patients with severe sepsis, who were hospitalizedin the Intensive Care Unit of Hospital General del Centro Médico Nacional,during five years.From these patients 107 developed acute renal failure due to severe sepsis. Thisgroup recived two differet kind of treatment, medical management (70%) and hemodyalisis(30%).Renal biopsy was taken in 40 patients after six or seven days of the diagnosisof acute renal failure caused by severe sepsis.Results: In the group of 332 patients with severe sepsis 107 developed acuterenal failure, this represents the 32.22%. The group of patients with renal biopsypresented the following results: 50% had acute tubular necrosis, 27.5% presentedglomerular and tubular lesion, the rest 22.5% had glomerular and vascular lesion.The mortality for patients treated with medical management was of 69.3%, andfor those treated with hemodyalisis was of 28.1%.Discussion: Nowadays, and due to the high incidence and mortality of this disease,is very important to generate more concise knowledge about the genesisand development of acute renal failure in the septic patient

Hydrocarbon biodegradation in oxygen-limited sequential batch reactors by consortium from weathered, oil-contaminated soil.

We studied the use of sequential batch reactors under oxygen limitation to improve and maintain consortium ability to biodegrade hydrocarbons. Air-agitated tubular reactors (2.5 L) were operated for 20 sequential 21-day cycles. Maya crude oil-paraffin mixture (13,000 mg/L) was used as the sole carbon source. The reactors were inoculated with a consortium from the rhizosphere of Cyperus laxus, a native plant that grows naturally in weathered, contaminated soil. Oxygen limitation was induced in the tubular reactor by maintaining low oxygen transfer coefficients (k(L)a < 20.6 h(-1)). The extent and biodegradation rates increased significantly up to the fourth cycle, maintaining values of about 66.33% and 460 mg x L(-1) x d(-1), respectively. Thereafter, sequential batch reactor operation exhibited a pattern with a constant general trend of biodegradation. The effect of oxygen limitation on consortium activity led to a low biomass yield and non-soluble metabolite (0.45 g SS/g hydrocarbons consumed). The average number of hydrocarbon-degrading microorganisms increased from 6.5 x 10(7) (cycles 1-3) to 2.2 x 10(8) (cycles 4-20). Five bacterial strains were identified: Achromobacter (Alcaligenes) xylosoxidans, Bacillus cereus, Bacillus subtilis, Brevibacterium luteum, and Pseudomonas pseudoalcaligenes. Asphaltene-free total petroleum hydrocarbons, extracted from a weathered, contaminated soil, were also biodegraded (97.1 mg x L(-1) x d(-1)) and mineralized (210.48 mg CO2 x L(-1) x d(-1)) by the enriched consortium without inhibition. Our results indicate that sequential batch reactors under oxygen limitation can be used to produce consortia with high and constant biodegradation ability for industrial applications of bioremediation.

[Neurological complications arising from dengue virus infection]. / Complicaciones neurológicas de la infección por el virus del dengue.

INTRODUCTION: Dengue is the most common of the arbovirosis that humans can suffer from. The frequency with which the central nervous system (CNS) is affected by this viral infection remains unknown, although isolated cases with neurological complications have been reported in Asia and South America. In Rio de Janeiro, Brazil, dengue virus infection has become an important public health concern. CASE REPORTS: The authors describe two cases of immune-mediated CNS involvement following classic infection by the dengue virus: one involving post-infectious disseminated acute encephalitis and the other consisting of Guillain-Barré syndrome. In both cases dengue was diagnosed using the ELISA technique, and other viral aetiologies in the cerebrospinal fluid (CSF) were excluded. A 10-year-old female, following a bout of classic dengue, presented symptoms of a diminished level of consciousness, spastic tetraparesis, cerebellar syndrome and frontal symptoms. A resonance brain scan showed areas of hypersignal in T2 sequences in the cerebral peduncle, lentiform nuclei and internal capsule on both sides of the brain, which suggested post-infectious encephalitis. The second patient, a 14-year-old male, presented an areflexive flaccid ascending tetraparesis that suggested acute polyradiculoneuritis, following a bout of classic dengue. CSF albuminocytologic dissociation was also observed. This patient's electroneuromyogram recording showed a polyradiculoneuropathy of a primarily demyelinating nature with an associated axonal component. CONCLUSIONS: The immunological mechanisms involved in the pathophysiology of this type of neurological complications after suffering from dengue may be part of the physiological response to the viral infection.

Glutamate release in the nucleus accumbens is involved in behavioral depression during the PORSOLT swim test.

An abnormality in glutamate function has been implicated in the neural substrate of depressive disorders. To investigate this in rats, the Porsolt swim test was used to assess the role of glutamate in the nucleus accumbens. Glutamate injected into the nucleus accumbens dose-dependently decreased swimming time on the test day (day 2), whereas N-methyl-D-aspartate antagonists dizocilpine and 2-amino-5-phosphonovalerate increased swimming, like an antidepressant. Dizocilpine injected before the conditioning trial (day 1) did not modify the swimming times during the first day but abolished behavioral depression on day 2. Microdialysis coupled to capillary-zone electrophoresis was then used to determine in vivo changes in glutamate release in 1-min samples during the swim test. On day 1, glutamate increased significantly and reached a maximum of 222% after 3 min of swimming. On day 2, baseline glutamate levels were back to normal, but when the animal was placed in the water, glutamate increased to 419% during the first minute, and the animals swam significantly less. For comparison, tail pinch on consecutive days was used as a nonspecific, repeated stressor while accumbens glutamate levels were measured. Tail pinch on the first day increased glutamate similar to the effect obtained during the first day of swimming; however, a second day of tail pinch decreased glutamate levels, instead of the potentiated response observed during the second day of swimming. These results show that accumbens glutamate plays a role in causing the behavioral aspects of depressed behavior as modeled in the swim test. The accumbens may be a potential site of action for drugs that alter behavioral depression.