Hydrodynamic disintegration of thickened excess sludge and maize silage to intensify methane production: Energy effect and impact on microbial communities.

The aim of this project was to study the combination of two methods to increase methane production: feedstock pretreatment by hydrodynamic disintegration and co-digestion of maize silage (MS) with thickened excess sludge (TES). Disintegration of TES alone resulted in a 15% increase in specific methane production from 0.192 Nml/gVS (TES + MS) to 0.220 Nml/gVS (pretreated TES + MS). The energy balance revealed additional energy (0.14 Wh) would cover only the energy expenditure for the mechanical pretreatment and would not allow for net energy profit. Identification of the methanogenic consortia by 16S rRNA gene amplicon sequencing revealed that Chloroflexi, Bacteroidota, Firmicutes, Proteobacteria and Actinobacteriota were five most abundant bacteria phyla, with Methanothrix and Methanolinea as the dominant methanogens. Principal component analysis did not show any effect of feedstock pretreatment on methanogenic consortia. Instead, the composition of inoculum was the decisive factor in shaping the microbial community structure.

Re-flocculation reduces the effectiveness of sewage sludge pretreatment through hydrodynamic disintegration prior to anaerobic digestion.

Circular economy model, based on the "make, use, reuse, remake, recycle" approach, is an alternative to progressive depletion of non-renewable fossil fuels. Sewage sludge can be a source of renewable energy obtained through the anaerobic conversion of their organic fraction into biogas. This process is mediated by highly complex microbial communities and its efficiency depends on the availability of substrates to microorganisms. Disintegration of the feedstock in the pre-treatment step may intensify the anaerobic digestion, but re-flocculation of disintegrated sludge (reassembly of the released fractions into larger agglomerates) may result in a reduced availability of the released organic compounds for microbes. Pilot-scale studies on re-flocculation of disintegrated sludge were conducted to select parameters for scaling-up the pre-treatment and intensifying the anaerobic digestion process in two large Polish wastewater treatment plants (WWTPs). Samples of thickened excess sludge from full-scale WWTPs were subjected to hydrodynamic disintegration at three energy density levels of 10 kJ/L, 35 kJ/L and 70 kJ/L. Microscopic analyses of disintegrated sludge samples were carried out twice: i) immediately after the disintegration process at a given energy density level, ii) and after 24-h incubation at 4 °C following the disintegration. Micro-photographs of 30 randomly selected fields of view were taken for each analysed sample. A method of the image analysis was developed as a tool to measure dispersion of sludge flocs to assess the re-flocculation degree. Re-flocculation of the thickened excess sludge occurred within 24 h after hydrodynamic disintegration. This was evidenced by a very high re-flocculation degree, reaching up to 86%, depending on the origin of the sludge and the energy density levels used for the hydrodynamic disintegration.

Cosmetic wastewater treatment with combined light/Fe0/H2O2 process coupled with activated sludge.

Wastewater from a cosmetic factory, with an initial chemical oxygen demand (COD) of 1140 mg/L, was treated using a combined light/Fe0/H2O2 process followed by biological treatment. The light/Fe0/H2O2 process, with 1000/2280 mg/L Fe0/H2O2 doses and 120 min process time, resulted in 70% COD removal, to final COD of 341 mg/L. The chemically treated wastewater was successfully subjected to biological treatment in a sequencing batch reactor (SBR), with up to 20% volume fraction in the influent, without significant deterioration of COD, nitrogen and phosphorus removal, but with possible small negative effects on polyphosphate accumulating organisms (PAOs), nitrifiers and other bacteria present in the microbial community. The COD of the effluent was in the range of 14-28 mg/L, resulting in overall COD removal of up to 97.7%. Untreated cosmetic wastewater, subjected to biological treatment in SBR, caused crucial changes in the microbial community structure, leading to a significant decrease in the efficiency of organic carbon, nitrogen and phosphorus removal.

Factors affecting population of filamentous bacteria in wastewater treatment plants with nutrients removal.

Filamentous population in activated sludge and key operational parameters of full-scale municipal wastewater treatment plants (WWTPs) with bulking problems representative for Poland were investigated with quantitative fluorescence in situ hybridization. Statistical analyses revealed few relationships between operational parameters and biovolume of filamentous bacteria. Sludge age was not only positively correlated with abundance of Chloroflexi (parametric correlation and principal component analysis (PCA)), but also differentiated Microthrix population (analysis of variance (ANOVA)). Phylum Chloroflexi and pH presented a negative relation during the study (PCA). ANOVA showed that pH of influent and sludge volume index (SVI) differentiated abundance of types 0803 and 1851 of Chloroflexi and candidate division TM7. SVI increased along with higher abundance of Microthrix (positive parametric and non-parametric correlations and positive relation in PCA). Biovolumes of morphotypes 0803 and 1851 of Chloroflexi were differentiated by organic matter in influent, also by nutrients in the case of Chloroflexi type 1851. Chemical and biological oxygen demands (COD and BOD5, respectively) were negatively correlated with Microthrix. COD also differentiated the abundance of Haliscomenobacter hydrossis. Results of the study can be used to prevent WWTPs from excessive proliferation of filamentous bacteria and operational problems caused by them--bulking and foaming of activated sludge.

The physiology of cardiac calcium handling.

Cardiac calcium (Ca(2+)) handling subsumes the mechanisms maintaining the myocardial Ca(2+) homeostasis that contribute essentially to cardiac performance. This review addresses the interaction of transplasmalemmal and transsarcoplasmic Ca(2+) flux, its potential modifications due to ß-adrenergic stimulation and its implications on cardiac action potential.

Proarrhythmia in a non-failing murine model of cardiac-specific Na+/Ca 2+ exchanger overexpression: whole heart and cellular mechanisms.

The cardiac Na(+)/Ca(2+) exchanger (NCX) generates an inward electrical current during SR-Ca(2+) release, thus possibly promoting afterdepolarizations of the action potential (AP). We used transgenic mice 12.5 weeks or younger with cardiomyocyte-directed overexpression of NCX (NCX-Tg) to study the proarrhythmic potential and mechanisms of enhanced NCX activity. NCX-Tg exhibited normal echocardiographic left ventricular function and heart/body weight ratio, while the QT interval was prolonged in surface ECG recordings. Langendorff-perfused NCX-Tg, but not wild-type (WT) hearts, developed ventricular tachycardia. APs and ionic currents were measured in isolated cardiomyocytes. Cell capacitance was unaltered between groups. APs were prolonged in NCX-Tg versus WT myocytes along with voltage-activated K(+) currents (K(v)) not being reduced but even increased in amplitude. During abrupt changes in pacing cycle length, early afterdepolarizations (EADs) were frequently recorded in NCX-Tg but not in WT myocytes. Next to EADs, delayed afterdepolarizations (DAD) triggering spontaneous APs (sAPs) occurred in NCX-Tg but not in WT myocytes. To test whether sAPs were associated with spontaneous Ca(2+) release (sCR), Ca(2+) transients were recorded. Despite the absence of sAPs in WT, sCR was observed in myocytes of both genotypes suggesting a facilitated translation of sCR into DADs in NCX-Tg. Moreover, sCR was more frequent in NCX-Tg as compared to WT. Myocardial protein levels of Ca(2+)-handling proteins were not different between groups except the ryanodine receptor (RyR), which was increased in NCX-Tg versus WT. We conclude that NCX overexpression is proarrhythmic in a non-failing environment even in the absence of reduced K(V). The underlying mechanisms are: (1) occurrence of EADs due to delayed repolarization; (2) facilitated translation from sCR into DADs; (3) proneness to sCR possibly caused by altered Ca(2+) handling and/or increased RyR expression.

Successful treatment of catecholaminergic polymorphic ventricular tachycardia with flecainide: a case report and review of the current literature.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic disease that can cause sudden cardiac death due to ventricular fibrillation (VF). While pharmacological therapy with beta-blockers and/or Ca(2)(+) antagonists is often unreliable, a recent study has demonstrated that flecainide can effectively suppress arrhythmia in a murine model of CPVT as well as clinically in two human subjects suffering from CPVT. We here present the case of an 11-year-old boy suffering from CPVT-1 as well as a review of the current relevant literature. After resuscitation due to VF at age 9, an automated implantable cardioverter-defibrillator (ICD) was implanted in 2007. Under beta-blocker therapy, repeated shocks were delivered due to either fast ventricular tachycardia (VT) or VF. This persisted under additional therapy with verapamil. Implantable cardioverter-defibrillator routine interrogations showed frequent non-sustained VT with an average of 8.8 per day. Additionally, the patient suffered from impaired physical performance due to decreased chronotropic competence. In July 2009, flecainide was added to the beta-blocker/verapamil regimen, resulting in a plasma level of 0.20 mg/L. No ICD shock or sustained VT occurred until December 2010. Genetic testing revealed an RyR2 receptor mutation. The case demonstrates the challenge of diagnosis and management of CPVT. It furthermore supports recent experimental evidence that the class 1 antiarrhythmic drug flecainide can suppress CPVT. The presented case supports a novel strategy in treating CPVT with the class I antiarrhythmic agent flecainide.