Microaerobic Digestion of Low-Biodegradable Sewage Sludge: Effect of Air Dosing in Batch Reactors

The adoption of prolonged solid retention times during the biological treatment of urban wastewaters is a well-known strategy to reduce sewage sludge production. However, it also results in the production of a biological sludge with low percentages of biodegradable organic matter, also characterized by high humification degrees, which may hamper the anaerobic digestion treatment aimed at sludge stabilization. To accelerate the hydrolytic stage, the application of microaerobic conditions during the anaerobic digestion of low-biodegradable sewage sludge was investigated in this study. In particular, six bio-methanation tests of a real sewage sludge were carried out, introducing air in the bioreactors with doses ranging between 0 and 16.83 L air/kg VSin d, in order to evaluate the air dosage that optimizes the biomethane production and organic matter degradation. Notably, the lower air loading rates investigated in this study, such as 0.68 and 1.37 L air/kg VSin d, led to an increase in methane production of up to 19%, due to a higher degradation of total lipids and proteins. In addition, these microaerobic conditions also resulted in a decrease in the sludge humification degree and in lower volatile fatty acid accumulation

Oxidized Low-Density Lipoproteins Induce Tissue Factor Expression in T-Lymphocytes via activation of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1

T-lymphocytes plays an important role in the pathophysiology of acute coronary syndromes (ACS). T-cell activation in vitro by pro-inflammatory cytokines may lead to functional Tissue Factor (TF) expression, indicating a possible contribution of immunity to thrombosis. Oxidized low-density lipoproteins (oxLDLs) are found abundantly in atherosclerotic plaques. We aimed at evaluating the effects of oxLDLs on TF expression in T-cells and the role of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1)

mGluR5 PAMs rescue cortical and behavioural defects in a mouse model of CDKL5 deficiency disorder

Cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) is a devastating rare neurodevelopmental disease without a cure, caused by mutations of the serine/threonine kinase CDKL5 highly expressed in the forebrain. CDD is characterized by early-onset seizures, severe intellectual disabilities, autistic-like traits, sensorimotor and cortical visual impairments (CVI). The lack of an effective therapeutic strategy for CDD urgently demands the identification of novel druggable targets potentially relevant for CDD pathophysiology. To this aim, we studied Class I metabotropic glutamate receptors 5 (mGluR5) because of their important role in the neuropathological signs produced by the lack of CDKL5 in-vivo, such as defective synaptogenesis, dendritic spines formation/maturation, synaptic transmission and plasticity. Importantly, mGluR5 function strictly depends on the correct expression of the postsynaptic protein Homer1bc that we previously found atypical in the cerebral cortex of Cdkl5-/y mice. In this study, we reveal that CDKL5 loss tampers with (i) the binding strength of Homer1bc-mGluR5 complexes, (ii) the synaptic localization of mGluR5 and (iii) the mGluR5-mediated enhancement of NMDA-induced neuronal responses. Importantly, we showed that the stimulation of mGluR5 activity by administering in mice specific positive-allosteric-modulators (PAMs), i.e., 3-Cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl)benzamide (CDPPB) or RO6807794, corrected the synaptic, functional and behavioral defects shown by Cdkl5-/y mice. Notably, in the visual cortex of 2 CDD patients we found changes in synaptic organization that recapitulate those of mutant CDKL5 mice, including the reduced expression of mGluR5, suggesting that these receptors represent a promising therapeutic target for CDD

Is it really advantageous to operate proximal femoral fractures within 48 h from diagnosis? – A multicentric retrospective study exploiting COVID pandemic-related delays in time to surgery

Objectives: Hip fractures in the elderly are common injuries that need timely surgical management. Since the beginning of the pandemic, patients with a proximal femoral fracture (PFF) experienced a delay in time to surgery. The primary aim of this study was to evaluate a possible variation in mortality in patients with PFF when comparing COVID-19 negative versus positive. Methods: This is a multicentric and retrospective study including 3232 patients with PFF who underwent surgical management. The variables taken into account were age, gender, the time elapsed between arrival at the emergency room and intervention, pre-operative American Society of Anesthesiology score, pre-operative cardiovascular and respiratory disease, and 10-day/1-month/6-month mortality. For 2020, we had an additional column, “COVID-19 swab positivity.” Results: COVID-19 infection represents an independent mortality risk factor in patients with PFFs. Despite the delay in time-to-surgery occurring in 2020, no statistically significant variation in terms of mortality was detected. Within our sample, a statistically significant difference was not detected in terms of mortality at 6 months, in patients operated within and beyond 48 h, as well as no difference between those operated within or after 12/24/72 h. The mortality rate among subjects with PFF who tested positive for COVID-19 was statistically significantly higher than in patients with PFF who tested. COVID-19 positivity resulted in an independent factor for mortality after PFF. Conclusion: Despite the most recent literature recommending operating PFF patients as soon as possible, no significant difference in mortality was found among patients operated before or after 48 h from diagnosis

Microaerobic Digestion of Low-Biodegradable Sewage Sludge: Effect of Air Dosing in Batch Reactors

The adoption of prolonged solid retention times during the biological treatment of urban wastewaters is a well-known strategy to reduce sewage sludge production. However, it also results in the production of a biological sludge with low percentages of biodegradable organic matter, also characterized by high humification degrees, which may hamper the anaerobic digestion treatment aimed at sludge stabilization. To accelerate the hydrolytic stage, the application of microaerobic conditions during the anaerobic digestion of low-biodegradable sewage sludge was investigated in this study. In particular, six bio-methanation tests of a real sewage sludge were carried out, introducing air in the bioreactors with doses ranging between 0 and 16.83 L air/kg VSin d, in order to evaluate the air dosage that optimizes the biomethane production and organic matter degradation. Notably, the lower air loading rates investigated in this study, such as 0.68 and 1.37 L air/kg VSin d, led to an increase in methane production of up to 19%, due to a higher degradation of total lipids and proteins. In addition, these microaerobic conditions also resulted in a decrease in the sludge humification degree and in lower volatile fatty acid accumulation

Sludge minimization in mainstream wastewater treatment: Mechanisms, strategies, technologies, and current development

: Excess sludge production in wastewater treatment plants has become an enormous environmental issue worldwide mainly due to the increased efforts towards wastewater purification. Researchers and plant operators are looking for technological solutions to reduce sludge production through the upgrading of existing technologies and configurations or by substituting them with alternative solutions. Several strategies have been identified to reduce sludge production, including the use of biological and physical-chemical methods (or a combination of them) and novel technologies, although many have not been sufficiently tested at full-scale. To select the most suitable system for sludge reduction, understanding the reduction mechanisms, advantages, disadvantages, and the economic and environmental impact of each technology is essential. This work offers a comprehensive and critical overview of mainstream sludge reduction technologies and underlying mechanisms from laboratory to full scale, and describes potential application, configuration, and integration with conventional systems. Research needs are highlighted, and a techno-economic-environmental comparison of the existing technologies is also proposed

Operational strategies enhancing sewage sludge minimization in a combined integrated fixed-film activated sludge - oxic settling anaerobic system

: A lab-scale integrated fixed-film activated sludge (IFAS) reactor was mplemented with the oxic-settling anaerobic (OSA) cycle for reducing sewage sludge production through the addition of an anoxic/anaerobic sludge holding tank (SHT) along the sludge recycle line. The IFAS-OSA system was operated under the different hydraulic retention time (HRT) in the SHT (HRTSHT) of 12 h and 6 h, at an oxidation-reduction potential (ORP) < -91 mV and solid retention time (SRT) between 39 and 126 d. Furthermore, the effect of temperature increase in the SHT (TSHT) from ambient (19.8-25.6 °C) to mesophilic (35 °C) conditions was investigated. The system performances were monitored in terms of sludge minimization and dewaterability efficiencies as well as carbon and nutrients reduction. The observed sludge yield (Yobs) for the IFAS system was 0.37(±0.06) mg VSS/mg COD. After OSA implementation Yobs decreased by 32% and 46-65% at HRTSHT of 12 h and 6 h, respectively, indicating that prolonged exposure to anoxic/anaerobic conditions was not beneficial for sludge reduction. The lowest Yobs of 0.09(±0.05) mg VSS/mg COD (76% lower than that in the IFAS system) was obtained at an HRTSHT of 6 h and when TSHT was set at 35 °C. OSA implementation did not affect COD and NH4+ oxidation of the IFAS system (90-96% and 99%, respectively) and improved total nitrogen (TN) reduction (31-53%) due to improved denitrification in the SHT. On the contrary, sludge dewaterability worsened following OSA implementation, which was linked to the increased levels of exopolymeric substances in the suspended biomass

Immune-inflammatory activation in acute coronary syndromes: A look into the heart of unstable coronary plaque

In the last twenty years, our comprehension of the molecular mechanisms involved in the formation, progression and complication of atherosclerotic plaque has advanced significantly and the main role of inflammation and immunity in this phenomenon is now largely accepted. Accumulating evidence highlight the crucial role of different inflammatory and immune cells, such as monocytes and T-lymphocytes, in the pathophysiology of atherosclerotic lesion, particularly in contributing to its complications, such as rupture or ulceration. According to the new terminology, \u201cvulnerable plaque\u201d identifies an inflamed atherosclerotic lesion that is particularly prone to rupture. Once disrupted, prothrombotic material is exposed to the flowing blood, thus activating coagulation cascade and platelet aggregation, ultimately leading to acute thrombus formation within the coronary vessel. To date this is the key event underlying the clinical manifestations of acute coronary syndromes (ACS). The degree of vessel occlusion (complete vs. incomplete) and the time of blood flow cessation will define the severity of clinical picture. This phenomenon seems to be the final effect of a complex interaction between different local and systemic factors, involving the degree of inflammation, type of cells infiltration and the rheological characteristics of blood flow at the site of plaque rupture, thrombogenic substrates within the atherosclerotic lesion and different soluble mediators, already present or acutely released in the circulating blood. This article will review currently available data on the pathophysiology of ACS, emphasizing the immunological and inflammatory aspects of vulnerable plaque. We may postulate that intraplaque antigens and local microenvironment will define the immune-inflammatory response and cells phenotype, thus determining the severity of clinical manifestations

Immune-inflammatory activation in acute coronary syndromes: A look into the heart of unstable coronary plaque

In the last twenty years, our comprehension of the molecular mechanisms involved in formation, progression and complication of atherosclerotic plaque has advanced significantly and the main role of inflammation and immunity in this phenomenon is now largely accepted. Accumulating evidence highlight the crucial role of different inflammatory and immune cells, such as monocytes and T-lymphocytes, in the pathophysiology of atherosclerotic lesion, particularly in contributing to its complications, such as rupture or ulceration. According to the new terminology, "vulnerable plaque" identifies an inflamed atherosclerotic lesion that is particularly prone to rupture. Once disrupted, prothrombotic material is exposed to the flowing blood, thus activating coagulation cascade and platelet aggregation, ultimately leading to acute thrombus formation within the coronary vessel. To date this is the key event underlying the clinical manifestation of acute coronary syndromes (ACS). The degree of vessel occlusion (complete vs. incomplete) and the time of blood flow cessation will define the severity of clinical picture. This phenomenon seems to be the final effect of a complex interaction between different local and systemic factors, involving the degree of inflammation, type of cells infiltration and the rheological characteristics of blood flow at the site of plaque rupture, thrombogenic substrates within the atherosclerotic lesion and different soluble mediators, already present or acutely released in the circulating blood. This article will review currently available data on the pathophysiology of ACS, emphasizing the immunological and inflammatory aspects of vulnerable plaque. We may postulate that intraplaque antigens and local microenvironment will define the immune-inflammatory response and cells phenotype, thus determining the severity of clinical manifestations.In the last twenty years, our comprehension of the molecular mechanisms involved in the formation, progression and complication of atherosclerotic plaque has advanced significantly and the main role of inflammation and immunity in this phenomenon is now largely accepted. Accumulating evidence highlight the crucial role of different inflammatory and immune cells, such as monocytes and T-lymphocytes, in the pathophysiology of atherosclerotic lesion, particularly in contributing to its complications, such as rupture or ulceration. According to the new terminology, “vulnerable plaque” identifies an inflamed atherosclerotic lesion that is particularly prone to rupture. Once disrupted, prothrombotic material is exposed to the flowing blood, thus activating coagulation cascade and platelet aggregation, ultimately leading to acute thrombus formation within the coronary vessel. To date this is the key event underlying the clinical manifestations of acute coronary syndromes (ACS). The degree of vessel occlusion (complete vs. incomplete) and the time of blood flow cessation will define the severity of clinical picture. This phenomenon seems to be the final effect of a complex interaction between different local and systemic factors, involving the degree of inflammation, type of cells infiltration and the rheological characteristics of blood flow at the site of plaque rupture, thrombogenic substrates within the atherosclerotic lesion and different soluble mediators, already present or acutely released in the circulating blood. This article will review currently available data on the pathophysiology of ACS, emphasizing the immunological and inflammatory aspects of vulnerable plaque. We may postulate that intraplaque antigens and local microenvironment will define the immune-inflammatory response and cells phenotype, thus determining the severity of clinical manifestations