Étude du processus de nitratation avec des boues activées : effet inhibiteur de l'ammoniac sur les bactéries nitratantes

Cet article porte sur l'étude de la réaction de nitratation (oxydation de nitrites en nitrates) par voie biologique aérobie avec des bactéries autotrophes nitratantes. Les phénomènes d'inhibition de l'ammoniac sur l'activité nitratante de populations microbiennes issues de boues activées (populations mixtes ou enrichies en bactéries nitratantes) ont été caractérisés.A l'aide d'une méthodologie faisant appel à la respirométrie, les caractéristiques de la population enrichie ont été définies :- les conditions optimales de mise en oeuvre sont un pH de 7,8 et une température de 29·C- les paramètres cinétiques définissant les performances sont QSmax=61 mgN-NO2-/gMVS×h et KS=3,04 mgN-NO2-/l- cette population présente une bonne tolérance vis-à-vis de NH3, une inhibition de 60% de la respiration des bactéries nitratantes ayant été obtenue pour 11,4 mgN-NH3/l.Les mêmes effets inhibiteurs ont été observés lors de la mise en culture discontinue de populations mixtes dans les conditions optimales de pH et température. Dans ces conditions de mise en oeuvre, différentes cultures dont les concentrations en biomasse totale ont varié de 0,1 à 2 gMVS/l, en présence de 3 mgN-NH3/l, ont présenté la même vitesse spécifique de nitratation. Ces phénomènes d'inhibition de la nitratation par NH3 paraissent complexes et fortement dépendant de facteurs environnementaux qui agissent sur la dynamique de croissance de ces bactéries.This paper focuses both on nitrification and on inhibition by ammonia of the bacteria responsible for this process in activated sludge (nitrifying bacteria). Nitrification (autotrophic nitrite oxidation to nitrate) is the limiting step in wastewater treatment plants during nitrogen biological treatment (ammonia is known as the major inhibitor). To assess the effects of environmental conditions on nitrification, respirometric measurements of a nitrifying bacteria-enriched activated sludge were carried out using a chemostat providing a stable nitrite-oxidizing population. The influence of pH, temperature, and the free ammonia concentration [NH3-N] was studied. The maximum activity of the nitrifying bacteria was found at pH 7.8 and at 29 oC, with the 90% range of maximum activity lying between pH values of 7.5 and 8.1. Activation and deactivation energies for nitrification were estimated by Arrhenius analysis to be 12.2 and - 41.5 kcal/mol, respectively. A Q10 value (multiplicative factor of oxygen consumption rate for each 10oC increase) of 2.8 was determined. Saturation or half-velocity coefficient (Ks) and maximum specific rate of nitrite oxidation (QSmax) were calculated by respirometric measurements, and are 3.04 mg NO2--N/l and 61 mg NO2--N/g VSS.h, respectively. In the study of effect of free ammonia, respirometric measurements were performed at ammonia concentrations ranging from 0.1 to 70 mg NH3-N/l. For a concentration of 11.4 mg NH3-N/l, a nitrification inhibition degree of 60% was reached. Contrary to the work of Anthonisen et al. (1976), which showed total inhibition of nitrifying bacteria at a concentration of 1 mg NH3-N/l, our results indicate a residual respiration, even at a concentration of 70 mg NH3-N/l. This displacement of total inhibition could be due to the predominance of nitrifying bacteria in the activated sludge used.In the second phase of the present research, our results were validated for another mixed bacterial population that was not enriched in nitrifying bacteria. Different concentrations of NH3 were imposed in flask cultures of nitrifying activated sludge, to assess the inhibition thresholds for ammonia. Between 0 and 10 mg NH3-N/l, the degrees of inhibition were inferior to those obtained by respirometric measurements for cultures enriched with nitrifying bacteria, except at 10 mg NH3-N/l, where about 58% inhibition was achieved. The effect of the total biomass concentration of nitrifying activated sludge was also studied. An ammonia concentration of 3 mg NH3-N/l was used in flask cultures with different biomass concentrations (0.1 to 2 g VSS/l). This variable was not significant as similar specific nitrite oxidation rates were measured in all cultures. Inhibitory effects of ammonia on nitrifying bacteria activity seem to be complex and strongly dependent on other environmental factors which modify the dynamics of biomass growth

FigGen: Text to Scientific Figure Generation

The generative modeling landscape has experienced tremendous growth in recent years, particularly in generating natural images and art. Recent techniques have shown impressive potential in creating complex visual compositions while delivering impressive realism and quality. However, state-of-the-art methods have been focusing on the narrow domain of natural images, while other distributions remain unexplored. In this paper, we introduce the problem of text-to-figure generation, that is creating scientific figures of papers from text descriptions. We present FigGen, a diffusion-based approach for text-to-figure as well as the main challenges of the proposed task. Code and models are available at https://github.com/joanrod/figure-diffusionComment: Published at ICLR 2023 as a Tiny Pape

Public Credit Programmes and Firm Performance in Brazil

Credit rationing is a common phenomenon faced by firms, one that has negative implications for longâ term investments. In Brazil, public credit plays a key role in supporting firms: stateâ owned banks account for almost half of the outstanding credit. Public credit programmes aim at reducing credit restrictions, increasing competitiveness and job creation for small and medium enterprises. This article analyzes the effectiveness of the credit lines managed by two main public institutions in Brazil. Results show that access to public credit lines has a significant positive impact on firmsâ employment growth and exports, while no effect was found on wage differential. The impact on exports is driven by the increase in volumes among exporting firms rather than the probability of becoming an exporter.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138401/1/dpr12250_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138401/2/dpr12250.pd

Insulin and GLP-1 infusions demonstrate the onset of adipose-specific insulin resistance in a large fasting mammal: potential glucogenic role for GLP-1.

Prolonged food deprivation increases lipid oxidation and utilization, which may contribute to the onset of the insulin resistance associated with fasting. Because insulin resistance promotes the preservation of glucose and oxidation of fat, it has been suggested to be an adaptive response to food deprivation. However, fasting mammals exhibit hypoinsulinemia, suggesting that the insulin resistance-like conditions they experience may actually result from reduced pancreatic sensitivity to glucose/capacity to secrete insulin. To determine whether fasting results in insulin resistance or in pancreatic dysfunction, we infused early- and late-fasted seals (naturally adapted to prolonged fasting) with insulin (0.065 U/kg), and a separate group of late-fasted seals with low (10 pM/kg) or high (100 pM/kg) dosages of glucagon-like peptide-1 (GLP-1) immediately following a glucose bolus (0.5g/kg), and measured the systemic and cellular responses. Because GLP-1 facilitates glucose-stimulated insulin secretion, these infusions provide a method to assess pancreatic insulin-secreting capacity. Insulin infusions increased the phosphorylation of insulin receptor and Akt in adipose and muscle of early and late fasted seals; however the timing of the signaling response was blunted in adipose of late fasted seals. Despite the dose-dependent increases in insulin and increased glucose clearance (high dose), both GLP-1 dosages produced increases in plasma cortisol and glucagon, which may have contributed to the glucogenic role of GLP-1. Results suggest that fasting induces adipose-specific insulin resistance in elephant seal pups, while maintaining skeletal muscle insulin sensitivity, and therefore suggests that the onset of insulin resistance in fasting mammals is an evolved response to cope with prolonged food deprivation