Nitrite (not free nitrous acid) is the main inhibitor of the anammox process at common pH conditions.

Nitrite is a substrate but also an inhibitor of anaerobic ammonium oxidation (anammox).There is currently no consensus on whether ionized nitrite (INi) or free nitrous acid (FNA) is the actual inhibitor of the process. The inhibition by INi and FNA on the anammox process has been analysed using a wide range of INi and FNA concentrations and by altering the pH and total nitrite conditions. The inhibitory impacts of both species were quantified through a rational inhibition equation, considering INi and FNA as substrate inhibitor and non-competitive inhibitor, respectively. Inhibitory constants were calculated with strong statistical support as 561 mg INi-N l(-1) and 0.117 mg FNA-N l(-1). Based on the model, INi is the main inhibiting species of the anammox process at pH > 7.1, which are the most common conditions occurring in field applications of anammox.

High pH (and not free ammonia) is responsible for Anammox inhibition in mildly alkaline solutions with excess of ammonium.

Ammonium is a substrate of the anaerobic ammonium oxidation (Anammox) process but it has been suggested as a substrate-inhibitor because of the action of its unionized form, free ammonia. High pH of the medium is also an important limiting factor of the Anammox bacteria. Both effects are difficult to discriminate. In this work the inhibitory effects of high pH, total ammonia (TA) and NH3 on the Anammox process were investigated simultaneously. Results confirmed that TA caused no inhibition and high pH is a much more important inhibiting factor than NH3 in mildly alkaline conditions, based on a multi-factorial analysis. Values of pH higher than 7.6 caused Anammox inhibition >10 % and should be avoided during the application of the Anammox process in practice.

Kinetics and thermodynamics of anaerobic ammonium oxidation process using Brocadia spp. dominated mixed cultures.

Anaerobic ammonium oxidation (anammox) is a recently discovered microbial process commonly applied to treat ammonium pollution in effluents with low organic carbon content. Modeling anammox processes is important for simulating and controlling full-scale plants. In this study, the anammox process was simulated using three models, and substrate and growth parameters obtained by different research groups. Two Brocadia spp.-dominated mixed cultures, one granular and the other flocculent, were used for this purpose. A very good correlation between experimental data using both sludges and model predictions was achieved by one of the models, obtaining correlation coefficients higher than 0.997. Other models and stoichiometric equations tested were unable to predict the anammox kinetics and stoichiometry. Furthermore, the thermodynamic behavior of the two mixed cultures was compared through the determination of the energy of activation of the anammox conversion at temperatures ranging from 9 to 40 °C. Optimum temperature for anammox activity was established at 30-35 °C in both cases. The energy of activation values calculated for granular sludge and flocculent sludge were 64 and 124 kJ mol(-1), respectively.

Anaerobic biodegradability of mixtures of pesticides in an expanded granular sludge bed reactor.

The biodegradability and toxicity of three commercial pesticides containing 2-methyl-4-chlorophenoxyacetic acid (MCPA), imidacloprid and dimethoate were evaluated individually, and a complex mixture of these pesticides was treated in an expanded granular sludge bed (EGSB) reactor. MCPA was partially biodegraded, while imidacloprid and dimethoate remained almost unaltered during the individual biodegradability tests. Cyclohexanone was identified as the major solvent in the dimethoate-bearing insecticide, which was completely removed regardless of the presence of other pesticides. The analysis of the inhibition over the acetoclastic methanogenesis showed IC(50) (half maximal inhibitory concentration) values of 474 and 367 mg/L for imidacloprid and dimethoate, respectively. The effect on the methanogenesis was negligible in the case of MCPA and cyclohexanone. Pesticides caused a dramatic decrease of the EGSB reactor performance. After 30 d acclimation, the EGSB reactor achieved a stable chemical oxygen demand (COD) removal efficiency and methane production of around 85% and 0.9 g CH(4)-COD/g COD, respectively, for MCPA, imidacloprid, dimethoate and cyclohexanone feed concentrations of 57, 20, 25 and 27 mg/L, respectively. The presence of complex pesticide mixtures led to synergistic/antagonistic responses, reducing the MCPA biodegradation and improving the removal of the insecticides' active ingredients, which were completely removed in the EGSB reactor.

Improvement of biogas production and nitrogen recovery in anaerobic digestion of purple phototrophic bacteria by thermal hydrolysis.

Purple phototrophic bacteria (PPB) are a novel driver to recover organics and nutrients from wastewater by assimilative growth. Depending on the source, assimilated resources from the PPB biomass can still be recovered after a releasing step. Anaerobic digestion (AD) releases carbonand nutrients, but the release is incomplete. Thermal hydrolysis (TH) as a pretreatment before AD improves the digestibility, release, and subsequent recovery potentials. This work determines the effects of TH in batch and continuous modes regarding methane potential, nutrients' release efficiencies, volatile solids destruction, degradability, and hydrolysis rates. Continuous runs over 165 days (d) confirmed enhanced recovery potentials, achieving up to 380 LCH4/kgVS (83 % solids destruction) and 73 % N release, respectively. The TH pretreatment is energy-intensive, but with appropriate heat recovery and increased methane production in the AD of the pretreated biomass, a combined configuration is energy positive.

The integrin beta1 modulator Tirofiban prevents adipogenesis and obesity by the overexpression of integrin-linked kinase: a pre-clinical approach in vitro and in vivo.

BACKGROUND: Obesity is caused by the enlargement of the white adipose tissue (WAT) depots, characterized by the hypertrophic enlargement of malfunctioning adipocytes within WAT which increases the storage of triglycerides (TG) in the lipid droplets (LD). Adipogenesis pathways as well as the expression and activity of some extracellular matrix receptors integrins are upregulated. Integrinß1 (INTB1) is the main isoform involved in WAT remodeling during obesity and insulin resistance-related diseases. We recently described Integrin Linked Kinase (ILK), a scaffold protein recruited by INTB1, as an important mediator of WAT remodeling and insulin resistance. As the few approved drugs to fight obesity have brought long-term cardiovascular side effects and given that the consideration of INTB1 and/or ILK modulation as anti-obesogenic strategies remains unexplored, we aimed to evaluate the anti-obesogenic capacity of the clinically approved anticoagulant Tirofiban (TF), stated in preclinical studies as a cardiovascular protector. METHODS: Fully differentiated adipocytes originating from C3H10T1/2 were exposed to TF and were co-treated with specific INTB1 blockers or with siRNA-based knockdown ILK expression. Lipid-specific dyes were used to determine the TG content in LD. The genetic expression pattern of ILK, pro-inflammatory cytokines (MCP1, IL6), adipogenesis (PPARγ, Leptin), thermogenesis (UCP1), proliferation (PCNA), lipid metabolism (FASN, HSL, ATGL), and metabolite transporters (FABP4, FAT, AQP7) were detected using quantitative PCR. Cytoskeletal actin polymerization was detected by confocal microscopy. Immunoblotting was performed to detect INTB1 phosphorylation at Thr788/9 and ILK activity as phosphorylation levels of protein kinase B (AKT) in Ser473 and glycogen synthase kinase 3ß (GSK3ß) at Ser9. TF was intraperitoneally administered once per day to wildtype and ILK knockdown mice (cKDILK) challenged with a high-fat diet (HFD) or control diet (STD) for 2 weeks. Body and WAT weight gains were compared. The expression of ILK and other markers was determined in the visceral epididymal (epi) and inguinal subcutaneous (sc) WAT. RESULTS: TF reduced TG content and the expression of adipogenesis markers and transporters in adipocytes, while UCP-1 expression was increased and the expression of lipases, cytokines or PCNA was not affected. Mechanistically, TF rapidly increased and faded the intracellular phosphorylation of INTB1 but not AKT or GSK3ß. F-actin levels were rapidly decreased, and INTB1 blockade avoided the TF effect. After 24 h, ILK expression and phosphorylation rates of AKT and GSK3ß were upregulated, while ILK silencing increased TG content. INTB1 blockade and ILK silencing avoided TF effects on the TG content and the transcriptional expression of PPARγ and UCP1. In HFD-challenged mice, the systemic administration of TF for several days reduced the weight gain on WAT depots. TF reduced adipogenesis and pro-inflammatory biomarkers and increased lipolysis markers HSL and FAT in epiWAT from HFD, while increased UCP1 in scWAT. In both WATs, TF upregulated ILK expression and activity, while no changes were observed in other tissues. In HFD-fed cKDILK, the blunted ILK in epiWAT worsened weight gain and avoided the anti-obesogenic effect of in vivo TF administration. CONCLUSIONS: ILK downregulation in WAT can be considered a biomarker of obesity establishment. Via an INTB1-ILK axis, TF restores malfunctioning hypertrophied WAT by changing the expression of adipocyte-related genes, increasing ILK expression and activity, and reducing TG storage. TF prevents obesity, a property to be added to its anticoagulant and cardiovascular protective advantages.

Fibronectin upregulates cGMP-dependent protein kinase type Iß through C/EBP transcription factor activation in contractile cells.

The nitric oxide (NO)-soluble guanylate cyclase (sGC) pathway exerts most of its cellular actions through the activation of the cGMP-dependent protein kinase (PKG). Accumulation of extracellular matrix is one of the main structural changes in pathological conditions characterized by a decreased activity of this pathway, such as hypertension, diabetes, or aging, and it is a well-known fact that extracellular matrix proteins modulate cell phenotype through the interaction with membrane receptors such as integrins. The objectives of this study were 1) to evaluate whether extracellular matrix proteins, particularly fibronectin (FN), modulate PKG expression in contractile cells, 2) to analyze the mechanisms involved, and 3) to evaluate the functional consequences. FN increased type I PKG (PKG-I) protein content in human mesangial cells, an effect dependent on the interaction with ß(1)-integrin. The FN upregulation of PKG-I protein content was due to increased mRNA expression, determined by augmented transcriptional activity of the PKG-I promoter region. Akt and the transcription factor CCAAT enhancer-binding protein (C/EBP) mediated the genesis of these changes. FN also increased PKG-I in another type of contractile cell, rat vascular smooth muscle cells (RVSMC). Tirofiban, a pharmacological analog of FN, increased PKG-I protein content in RVSMC and rat aortic walls and magnified the hypotensive effect of dibutyryl cGMP in conscious Wistar rats. The present results provide evidence of a mechanism able to increase PKG-I protein content in contractile cells. Elucidation of this novel mechanism provides a rationale for future pharmacotherapy in certain vascular diseases.

Anaerobic biodegradation of 2,4,6-trichlorophenol in expanded granular sludge bed and fluidized bed biofilm reactors bioaugmented with Desulfitobacterium spp.

The biodegradation of 2,4,6-trichlorophenol (246TCP) was studied using expanded granular sludge bed (EGSB) reactors and a fluidized bed biofilm reactor (FBBR) filled with activated carbon. One of the EGSB reactor and the FBBR were bioaugmented with Desulfitobacterium strains. 246TCP loading rate was gradually incremented from 10 to 250 mg L(-1) day(-1). The main pathway of dechlorination was in ortho-position, generating 4-chlorophenol and 2,4-dichlorophenol. The maintenance of both COD degradation efficiency (higher than 80%) and methanogenic efficiency (between 0.3 and 0.6 g CH4-COD g(-1) COD consumed) in EGSB reactor implies a great stability of the process. Through isotherm studies in FBBR, it could be deduced that around 52% of 246TCP was completely dechlorinated, whereas the adsorption involved around 16%. By means of FISH studies it was proved that the methanogenic Archaea community was maintained in the bioaugmented EGSB reactor, whereas in the FBBR this community was gradually developed until reaching stability. Desulfitobacterium community was also maintained in the reactors, although D. chlororespirans proportion rise in the FBBR at the higher 246TCP loading rates, implying that this species can withstand the 246TCP toxicity better than D. hafniense.

Up-scale challenges on biopolymer production from waste streams by Purple Phototrophic Bacteria mixed cultures: A critical review.

The increasing volume of waste streams require new biological technologies that can address pollution concerns while offering sustainable products. Purple phototrophic bacteria (PPB) are very versatile organisms that present a unique metabolism that allows them to adapt to a variety of environments, including the most complex waste streams. Their successful adaptation to such demanding conditions is partly the result of internal polymers accumulation which can be stored for electron/energy balance or as carbon and nutrients reserves for deprivation periods. Polyhydroxyalkanoates, glycogen, sulphur and polyphosphate are examples of polymers produced by PPB that can be economically explored due to their applications in the plastic, energy and fertilizers sectors. Their large-scale production implies the outdoor operation of PPB systems which brings new challenges, identified in this review. An overview of the current PPB polymer producing technologies and prospects for their future development is also provided.

Exploring the inhibition boundaries of mixed cultures of purple phototrophic bacteria for wastewater treatment in anaerobic conditions.

The development of novel wastewater platforms should include the analysis of the most critical functional factors including the effects of toxic or inhibitory substances. Due to the novelty of purple phototrophic bacteria (PPB)-based wastewater treatment systems, this analysis has not been done yet in mixed cultures. In this work, various relevant chemical compounds, including aromatic (phenol, 2,4,6-trichlorophenol or 246TCP, 4-nitrophenol or 4CP, sulfathiazole) and aliphatic organics (methanol, trichlorethylene or TCE, oleic acid, ethanol, propionic acid), inorganic salts (ammonium, ClO3-, Na+), and metals (Fe3+, Fe2+, Cu2+, Zn2+, Ni2+, Al3+), as well as pH, are analyzed for their effect on mixed PPB cultures in anaerobic photoheterotrophic conditions using acetate as the model organic substrate. The most toxic substances detected were 246TCP, 4NP, Cu2+, Fe2+ and Ni2+, (Ki for activity: 23 ± 2, 97 ± 12, 3.1 ± 0.4, 13 ± 3, 13 ± 1 mg/L, and Ki (or toxicity threshold) for growth: 17 ± 2, (119), 3.5 ± 0.4, (4.8), (22.9) mg/L, respectively). Some substances inhibited the activity more than the growth (sulfathiazole, Ni2+ and Fe3+), or the growth more than the activity (TCE, 4NP and Fe2+). In addition, some organic substrates, such as phenol, ethanol and propionate, specifically inhibited the acetate uptake, being noncompetitive in the case of phenol and ethanol, and most likely competitive in the case of propionate. These findings are relevant for the wastewater treatment and resource recovery applications of the PPB technology, as well as for the upgrading of current models (Photo-Anaerobic Model). In addition, the data will open possibilities to promote the production of specific compounds (as PHA or single-cell proteins) by selectively inhibiting some parts of the PPB metabolism.

Contamination of N-poor wastewater with emerging pollutants does not affect the performance of purple phototrophic bacteria and the subsequent resource recovery potential.

Propagation of emerging pollutants (EPs) in wastewater treatment plants has become a warning sign, especially for novel resource-recovery concepts. The fate of EPs on purple phototrophic bacteria (PPB)-based systems has not yet been determined. This work analyzes the performance of a photo-anaerobic membrane bioreactor treating a low-N wastewater contaminated with 25 EPs. The chemical oxygen demand (COD), N and P removal efficiencies were stable (76 ±â€¯8, 62 ±â€¯15 and 36 ±â€¯8 %, respectively) for EPs loading rate ranging from 50 to 200 ng L-1 d-1. The PPB community adapted to changes in both the EPs concentration and the organic loading rate (OLR) and maintained dominance with >85 % of total 16S gene copies. Indeed, an increment of the OLR caused an increase of the biomass growth and activity concomitantly with a higher EPs removal efficiency (30 ±â€¯13 vs 54 ±â€¯11 % removal for OLR of 307 ±â€¯4 and 590 ±â€¯8 mgCOD L-1 d-1, respectively). Biodegradation is the main mechanism of EPs removal due to low EPs accumulation on the biomass, the membrane or the reactor walls. Low EPs adsorption avoided biomass contamination, resulting in no effect on its biological methane potential. These results support the use of PPB technologies for resource recovery with low EPs contamination of the products.

Safety and Tolerability of Tolvaptan in an Autosomal Dominant Polycystic Kidney Disease Spanish Cohort: A Real-World Experience.

INTRODUCTION: Autosomal dominant polycystic kidney disease (ADPKD) is the commonest inherited disorder of the kidneys. A vasopressin V2-receptor antagonist (tolvaptan) was recently approved for the treatment of ADPKD. This study aims to analyze the safety and tolerability of tolvaptan for the management of ADPKD patients in a real-world setting. METHODS: We conducted a descriptive retrospective study in ADPKD patients in an outpatient clinic setting in Spain from 2018 to 2019. Descriptive statistical analysis of demographics and clinical data, at baseline and one year after tolvaptan initiation, was assessed. Data are presented as median and interquartile range, and as frequencies for categorical variables. RESULTS: Ten patients with ADPKD were identified. At baseline median age was 49.5 (38.5-63.5) years and 60% were males. During treatment with tolvaptan, no significant aquaresis-related symptoms or hepatotoxicity were described. No serious adverse events, discontinuation, or deaths were reported during the study. CONCLUSION: Tolvaptan was well-tolerated without severe adverse events in patients with ADPKD who showed rapid disease progression criteria. Longer follow-up is required to learn about the long-term effects of this treatment.

Anaerobic biodegradation of 2,4,6-trichlorophenol by methanogenic granular sludge: role of co-substrates and methanogenic inhibition.

The influence of several co-substrates in the anaerobic biodegradation of 2,4,6-trichlorophenol (246TCP) by methanogenic granular sludge as well as in methanogenesis inhibition by 246TCP has been studied. 4 g-COD.L(-1) of lactate, sucrose, volatile fatty acids (VFA) acetate:propionate:butyrate 1:1:1, ethanol, methanol, yeast extract (YE), and 2 g-COD.L(-1) of formate and methylamine were tested. Two concentrations of 246TCP: 80 mg.L(-1) and 113 mg.L(-1) (this last corresponding to the EC(50) for acetotrophic methanogenesis) were tested. Three consecutive co-substrate and nutrient feedings were accomplished. 246TCP was added in the second feed, and the 246TCP removal rate increased considerably after the third feed. Accumulated metabolites after ortho-dechlorination, either 4-chlorophenol (4CP) (when methanol, ethanol or VFA were used as co-substrates) or 2,4-dichlorophenol (24DCP) (with lactate) avoided the complete dechlorination of 246TCP. With methylamine and formate this compound was degraded only partially. Monochlorophenols biodegradation was partially achieved with YE, but both 24DCP and 2,6-dichlorophenol (26DCP) were accumulated. In the presence of sucrose para-dechlorination was observed. 246TCP was better tolerated by methanogens when ethanol and methanol were added because of the highest specific methanogenic activity achieved with these co-substrates. Methanol and ethanol were the best co-substrates in the anaerobic biodegradation of 246TCP.

Role of activator protein-1 on the effect of arginine-glycine-aspartic acid containing peptides on transforming growth factor-beta1 promoter activity.

While arginine-glycine-aspartic acid-based peptidomimetics have been employed for the treatment of cardiovascular disorders and cancer, their use in other contexts remains to be explored. Arginine-glycine-aspartic acid-serine induces Transforming growth factor-beta1 transcription in human mesangial cells, but the molecular mechanisms involved have not been studied extensively. We explored whether this effect could be due to Activator protein-1 activation and studied the potential pathways involved. Addition of arginine-glycine-aspartic acid-serine promoted Activator protein-1 binding to its cognate sequence within the Transforming growth factor-beta1 promoter as well as c-jun and c-fos protein abundance. Moreover, this effect was suppressed by curcumin, a c-Jun N terminal kinase inhibitor, and was absent when the Activator protein-1 cis-regulatory element was deleted. Activator protein-1 binding was dependent on the activity of integrin linked kinase, as transfection with a dominant negative mutant suppressed both Activator protein-1 binding and c-jun and c-fos protein increment. Integrin linked kinase was, in turn, dependent on Phosphoinositol-3 kinase activity. Arginine-glycine-aspartic acid-serine stimulated Phosphoinositol-3 kinase activity, and Transforming growth factor-beta1 promoter activation was abrogated by the use of Phosphoinositol-3 kinase specific inhibitors. In summary, we propose that arginine-glycine-aspartic acid-serine activates Integrin linked kinase via the Phosphoinositol-3 kinase pathway and this leads to activation of c-jun and c-fos and increased Activator protein-1 binding and Transforming growth factor-beta1 promoter activity. These data may contribute to understand the molecular mechanisms involved in the cellular actions of arginine-glycine-aspartic acid-related peptides and enhance their relevance as these products evolve into clinical therapeutic use.

The peptidase inhibitor CGS-26303 increases endothelin converting enzyme-1 expression in endothelial cells through accumulation of big endothelin-1.

BACKGROUND AND PURPOSE: CGS-26303 inhibits endothelin converting enzyme (ECE)-1 more specifically than phosphoramidon. We have studied the effect of CGS-26303 on ECE-1 expression in bovine aortic endothelial cells. METHODS: ECE-1 activity and big endothelin (ET)-1 levels were measured by ELISA, ECE-1 expression using western and northern blot and promoter activity using transfection assays. KEY RESULTS: ECE-1 activity was completely inhibited by CGS-26303 25 microM and phosphoramidon 100 microM. CGS-26303 and phosphoramidon, though not thiorphan, a neutral endopeptidase (NEP) inhibitor, stimulated ECE-1 expression in cells (maximal effect at 16 h, 25 microM). Cycloheximide abolished that effect. CGS-26303 induced ECE-1 mRNA expression and ECE-1 promoter activity. CGS-35066, a selective ECE-1 inhibitor, mimicked the effects of CGS-26303, suggesting that the effect was specific to ECE-1 inhibition. Big ET-1 accumulated in the cells and in the supernatants after CGS-26303 treatment. Neither exogenously added ET-1 nor the blockade of their receptors with bosentan modified ECE-1 protein. When big ET-1 was added to cells, significant increases in ECE-1 protein content and ECE-1 promoter activity were found. Bosentan did not block those effects. CGS-26303 did not modify prepro-ET-1 expression. CGS-26303 and big ET-1 induced the same effects in human endothelial cells, at lower doses. CONCLUSIONS: These results suggest that the accumulation of big ET-1 is responsible for the effects of CGS-26303 on ECE-1 and they did not depend on NEP blockade. Changes in ECE-1 protein after the administration of CGS-26303 could lead to a decreased response in long-term treatments.

[Differences in the synthesis pattern of vasoactive factors in gestational hypertension and preeclampsia]. / Diferencias en el patrón de síntesis de factores vasoactivos en la hipertensión gestacional y en la preeclampsia.

BACKGROUND AND OBJECTIVE: The gestational hypertension -HG- and preeclampsia -P- are hypertensive diseases whose pathogenic mechanism has not been determined yet. The aim of this work is to define some patterns of vasoactive factors release that allow to explain the origin of the differences between both entities. DESIGN: Prospective case-control study. MATERIAL AND METHODS: Two groups of target patients were consecutively selected, GH (n=21) and P patients (n=21). Every patient was matched with a pregnant of similar age and week of pregnancy. Two control groups were obtained, one respect to the GH and another one respect to the P group. A biochemistry, blood cell count, coagulation and quantification of vasoactive factors endothelin, nitrites and GMPc were performed in every woman. Results of GH and P groups were compared with their respective control group with the paired Student's t Test. RESULTS: Both systolic and diastolic arterial pressures were higher in hypertensive pregnants (GH and P) than in their respective controls. Moreover, blood endothelin and GMPc were higher in GH and P. GH pregnants showed decreased norepinephrine and increased epinephrine urinary excretion , as well as an increased plasma nitrites concentration than control group. P patients did not show statistically significant differences in catecholamines urinary excretion nor in plasma nitrites concentration respect their control group. CONCLUSION: There are relevant differences in the synthesis patterns of vasoactive factors between gestational hypertension and preeclampsia. These differences could account for a decreased tissue perfusion in preeclampsia and could also contribute to the genesis of the renal dysfunction of this entity.

A mechanistic model for anaerobic phototrophs in domestic wastewater applications: Photo-anaerobic model (PAnM).

Purple phototrophic bacteria (PPB) have been recently proposed as a key potential mechanism for accumulative biotechnologies for wastewater treatment with total nutrient recovery, low greenhouse gas emissions, and a neutral to positive energy balance. Purple phototrophic bacteria have a complex metabolism which can be regulated for process control and optimization. Since microbial processes governing PPB metabolism differ from traditional processes used for wastewater treatment (e.g., aerobic and anaerobic functional groups in ASM and ADM1), a model basis has to be developed to be used as a framework for further detailed modelling under specific situations. This work presents a mixed population phototrophic model for domestic wastewater treatment in anaerobic conditions. The model includes photoheterotrophy, which is divided into acetate consumption and other organics consumption, chemoheterotrophy (including simplified fermentation and anaerobic oxidation) and photoautotrophy (using hydrogen as an electron donor), as microbial processes, as well as hydrolysis and biomass decay as biochemical processes, and is single-biomass based. The main processes have been evaluated through targeted batch experiments, and the key kinetic and stoichiometric parameters have been determined. The process was assessed by analyzing a continuous reactor simulation scenario within a long-term wastewater treatment system in a photo-anaerobic membrane bioreactor.

Enhanced anaerobic degradability of highly polluted pesticides-bearing wastewater under thermophilic conditions.

This work presents a sustainable and cost-competitive solution for hardly biodegradable pesticides-bearing wastewater treatment in an anaerobic expanded granular sludge bed (EGSB) reactor at mesophilic (35°C) and thermophilic (55°C). The reactor was operated in continuous mode during 160days, achieving an average COD removal of 33 and 44% under mesophilic and thermophilic conditions, respectively. The increase of temperature improved the biomass activity and the production of methane by 35%. Around 96% of pesticides identified in raw wastewater were not detected in both mesophilic and thermophilic effluents. A dramatic selection of the microbial population in anaerobic granules was caused by the presence of pesticides, which also changed significantly when the temperature was increased. Pesticides caused a significant inhibition on methanogenesis, especially over acetoclastic methanogens. Aerobic biodegradability tests of the resulting anaerobic effluents revealed that aerobic post-treatment is also a feasible and effective option, yielding more than 60% COD reduction.

Decreased nitric oxide synthesis in human endothelial cells cultured on type I collagen.

Endothelial dysfunction, considered as a defective vascular dilatation after certain stimuli, is characteristic of different pathological conditions, such as hypertension, atherosclerosis, or diabetes. A decreased synthesis or an increased degradation of nitric oxide (NO) has been postulated as the mechanism responsible for this alteration. The present experiments were designed to test the hypothesis that the presence of an abnormal extracellular matrix in vessel walls could be responsible for the decreased NO synthesis observed in these pathological conditions. Experiments were performed in cultured human umbilical vein endothelial cells (HUVECs) grown on type IV (Col. IV) or type I (Col. I) collagen. Cells seeded on Col. I showed decreased nitrite synthesis, nitric oxide synthase activity, eNOS protein content, and eNOS mRNA expression when compared with cells grown on Col. IV. Moreover, cells grown on Col. I failed to respond to glucose oxidase activation of the eNOS system. In both cases, the changes in the eNOS mRNA expression seemed to depend on the modulation of eNOS promoter activity. The downregulation of eNOS induced by Col. I was blocked by D6Y, a peptide that interferes with the Col. I-dependent signals through integrins, as well as by specific anti-integrin antibodies. Moreover, a decreased activation of integrin-linked kinase (ILK) may explain the effects observed in Col. I-cultured cells because the activity of this kinase was decreased in these cells and ILK modulation prevented the Col. I-induced changes in HUVECs. Taken together, these findings may contribute to explaining the basis of endothelial dysfunction in some vascular diseases.