Dewatering of excess sludge produced by cas and mbr aerobic treatment plants. effects of biochemical stability and eps composition

This paper investigates the behavior of different sludges from several treatment plants at full and pilot scale configured as Conventional Activated Sludge (CAS) and Membrane Bio Reactor (MBR) plants treating different kinds of wastewaters. The sludges collected were subjected to complete analytical and technological characterization in order to correlate the rheological properties that affect the dewatering behavior to the sludge chemical physical properties. In detail the EPS from the samples collected is extracted and characterized in terms of carbohydrates, proteins, uronic acids and humic acids content. Moreover, once characterized, the sludges were subjected to AD in order to assess their bio-methanation potential and hence their biological stability. The final aim was to find correlations between the WWTP operational parameters (i.e. HRT, SRT, volumetric load coefficient, aeration) that finally affect its chemical composition (i.e. BMP, EPS composition) and the physical behavior of the sludge

Skeletal muscle derived Musclin protects the heart during pathological overload

Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy

TOWARDS A REDUCTION OF GREENHOUSE GAS EMISSION FROM WASTEWATER TREATMENT EMISSION FROM WASTEWATER TREATMENT PLANTS: A NEW PLANT WIDE EXPERIMENTAL AND MODELLING APPROACH

The increasing interest in greenhouse gas (GHG) emissions from wastewater treatment plants (WWTPs) has led to the development of new tools for their design and management. Studies about gas emissions show that the sewer collection and the wastewater treatment plant are anthropogenic GHG potential sources, so they contribute to the climate change and air pollution. A wastewater treatment plant receives wastewater from sewers and, while produces treated water for discharge into surface water, emits the three major greenhouse gases, CO2, CH4, and N2O, during the treatment processes, and additional amounts of CO2 and CH4 from the energy demands (Bani Shahabadi et al., 2009). Indeed, energy consumption can be considered as an indirect source of GHGs. Greenhouse-gas emissions are generated by water-line and sludge-line processes and by the on-site combustion of biogas and fossil fuels for energy generation. GHGs may also be produced during sludge disposal or reuse (transportation and degradation of remaining biosolids off-site), off-site energy production and off-site chemicals production. In recent years, increasing attention is given to the assessment of N2O emissions from WWTPs. N2O is a powerful greenhouse gas that is almost 300 times stronger than CO2. Nevertheless, the source and magnitude of N2O are relatively unknown and the knowledge is still incomplete. This paper presents the first results of an ongoing research project aiming at setting-up an innovative mathematical model platform (Decision Support System—DSS) for the design and management of WWTPs. The project is constituted by four research units (UOs) and its final goal is to minimize, by means of this platform, the environmental impact of WWTPs through their optimization in terms of energy consumptions and pollutants, sludge and GHG emissions

Toward a New Plant-Wide Experimental and Modeling Approach for Reduction of Greenhouse Gas Emission from Wastewater Treatment Plants

Mechanisms causing greenhouse gas (GHG) emission in wastewater treatment plants are of great interest among researchers, encouraging the development of new methods for wastewater management. Wastewater treatment plants (WWTPs) emit three major greenhouse gases during the treatment processes: CO2, CH4, and N2O. Additional amounts of CO2 and CH4 are produced during energy consumption, which can be considered an indirect source of GHGs. Recently, several efforts have been undertaken to assess GHGs from WWTPs, with particular attention paid to the N2O assessment due to its high warming potential (300 times stronger than CO2). This study proposes an integrated model platform for WWTP simulation, including the evaluation of both direct and indirect emissions as plant performance parameters. The results of extensive research demonstrate the importance of mathematical modeling for the development of a decision support system (DSS). The project involves four research units (RUs) united in effort to minimize the environmental impact of wastewater treatment plants in terms of both energy consumption and discharged pollutants (solids, liquids, and gases)

Endothelial cells drive organ fibrosis in mice by inducing expression of the transcription factor SOX9

Fibrosis is a hallmark of chronic disease. Although fibroblasts are involved, it is unclear to what extent endothelial cells also might contribute. We detected increased expression of the transcription factor Sox9 in endothelial cells in several different mouse fibrosis models. These models included systolic heart failure induced by pressure overload, diastolic heart failure induced by high-fat diet and nitric oxide synthase inhibition, pulmonary fibrosis induced by bleomycin treatment, and liver fibrosis due to a choline-deficient diet. We also observed up-regulation of endothelial SOX9 in cardiac tissue from patients with heart failure. To test whether SOX9 induction was sufficient to cause disease, we generated mice with endothelial cell–specific overexpression of Sox9 , which promoted fibrosis in multiple organs and resulted in signs of heart failure. Endothelial Sox9 deletion prevented fibrosis and organ dysfunction in the two mouse models of heart failure as well as in the lung and liver fibrosis mouse models. Bulk and single-cell RNA sequencing of mouse endothelial cells across multiple vascular beds revealed that SOX9 induced extracellular matrix, growth factor, and inflammatory gene expression, leading to matrix deposition by endothelial cells. Moreover, mouse endothelial cells activated neighboring fibroblasts that then migrated and deposited matrix in response to SOX9, a process partly mediated by the secreted growth factor CCN2, a direct SOX9 target; endothelial cell–specific Sox9 deletion reversed these changes. These findings suggest a role for endothelial SOX9 as a fibrosis-promoting factor in different mouse organs during disease and imply that endothelial cells are an important regulator of fibrosis.SOX9 in endothelial cells regulates organ fibrosis in mice by inducing extracellular matrix, inflammatory, and growth factor gene expression.Editor’s summary Chronic disease is often characterized by organ fibrosis, but how specific cell types contribute to fibrosis is unclear. Here, Trogisch et al. showed that endothelial cells are important drivers of fibrosis in heart failure, pulmonary fibrosis, and liver fibrosis mouse models. Up-regulation of the transcription factor SOX9 specifically in endothelial cells was associated with organ fibrosis in these mouse models. Overexpression of endothelial SOX9 resulted in fibrosis pathology in multiple mouse organs, whereas deletion of SOX9 in endothelial cells prevented organ fibrosis and dysfunction. SOX9 was also increased in cardiac tissue from patients with heart failure, suggesting that endothelial cell SOX9 may be a therapeutic target for human fibrotic disease. —Brandon BerryFibrosis is a hallmark of chronic disease. Although fibroblasts are involved, it is unclear to what extent endothelial cells also might contribute. We detected increased expression of the transcription factor Sox9 in endothelial cells in several different mouse fibrosis models. These models included systolic heart failure induced by pressure overload, diastolic heart failure induced by high-fat diet and nitric oxide synthase inhibition, pulmonary fibrosis induced by bleomycin treatment, and liver fibrosis due to a choline-deficient diet. We also observed up-regulation of endothelial SOX9 in cardiac tissue from patients with heart failure. To test whether SOX9 induction was sufficient to cause disease, we generated mice with endothelial cell–specific overexpression of Sox9 , which promoted fibrosis in multiple organs and resulted in signs of heart failure. Endothelial Sox9 deletion prevented fibrosis and organ dysfunction in the two mouse models of heart failure as well as in the lung and liver fibrosis mouse models. Bulk and single-cell RNA sequencing of mouse endothelial cells across multiple vascular beds revealed that SOX9 induced extracellular matrix, growth factor, and inflammatory gene expression, leading to matrix deposition by endothelial cells. Moreover, mouse endothelial cells activated neighboring fibroblasts that then migrated and deposited matrix in response to SOX9, a process partly mediated by the secreted growth factor CCN2, a direct SOX9 target; endothelial cell–specific Sox9 deletion reversed these changes. These findings suggest a role for endothelial SOX9 as a fibrosis-promoting factor in different mouse organs during disease and imply that endothelial cells are an important regulator of fibrosis.SOX9 in endothelial cells regulates organ fibrosis in mice by inducing extracellular matrix, inflammatory, and growth factor gene expression.Editor’s summary Chronic disease is often characterized by organ fibrosis, but how specific cell types contribute to fibrosis is unclear. Here, Trogisch et al. showed that endothelial cells are important drivers of fibrosis in heart failure, pulmonary fibrosis, and liver fibrosis mouse models. Up-regulation of the transcription factor SOX9 specifically in endothelial cells was associated with organ fibrosis in these mouse models. Overexpression of endothelial SOX9 resulted in fibrosis pathology in multiple mouse organs, whereas deletion of SOX9 in endothelial cells prevented organ fibrosis and dysfunction. SOX9 was also increased in cardiac tissue from patients with heart failure, suggesting that endothelial cell SOX9 may be a therapeutic target for human fibrotic disease. —Brandon BerryFibrosis is a hallmark of chronic disease. Although fibroblasts are involved, it is unclear to what extent endothelial cells also might contribute. We detected increased expression of the transcription factor Sox9 in endothelial cells in several different mouse fibrosis models. These models included systolic heart failure induced by pressure overload, diastolic heart failure induced by high-fat diet and nitric oxide synthase inhibition, pulmonary fibrosis induced by bleomycin treatment, and liver fibrosis due to a choline-deficient diet. We also observed up-regulation of endothelial SOX9 in cardiac tissue from patients with heart failure. To test whether SOX9 induction was sufficient to cause disease, we generated mice with endothelial cell–specific overexpression of Sox9 , which promoted fibrosis in multiple organs and resulted in signs of heart failure. Endothelial Sox9 deletion prevented fibrosis and organ dysfunction in the two mouse models of heart failure as well as in the lung and liver fibrosis mouse models. Bulk and single-cell RNA sequencing of mouse endothelial cells across multiple vascular beds revealed that SOX9 induced extracellular matrix, growth factor, and inflammatory gene expression, leading to matrix deposition by endothelial cells. Moreover, mouse endothelial cells activated neighboring fibroblasts that then migrated and deposited matrix in response to SOX9, a process partly mediated by the secreted growth factor CCN2, a direct SOX9 target; endothelial cell–specific Sox9 deletion reversed these changes. These findings suggest a role for endothelial SOX9 as a fibrosis-promoting factor in different mouse organs during disease and imply that endothelial cells are an important regulator of fibrosis.SOX9 in endothelial cells regulates organ fibrosis in mice by inducing extracellular matrix, inflammatory, and growth factor gene expression.Editor’s summary Chronic disease is often characterized by organ fibrosis, but how specific cell types contribute to fibrosis is unclear. Here, Trogisch et al. showed that endothelial cells are important drivers of fibrosis in heart failure, pulmonary fibrosis, and liver fibrosis mouse models. Up-regulation of the transcription factor SOX9 specifically in endothelial cells was associated with organ fibrosis in these mouse models. Overexpression of endothelial SOX9 resulted in fibrosis pathology in multiple mouse organs, whereas deletion of SOX9 in endothelial cells prevented organ fibrosis and dysfunction. SOX9 was also increased in cardiac tissue from patients with heart failure, suggesting that endothelial cell SOX9 may be a therapeutic target for human fibrotic disease. —Brandon Berr