Effect of KMnO4/pH adjustment of extracellular polymeric substances under waste activated sludge on sludge dewatering.

In this study, we examine the dewaterability of sludge after treatment by KMnO4 at various pH levels, with the goal of understanding the dewaterability of strong oxidizers to waste activated sludge. Good dewatering performance is observed, with capillary suction times (CST) reduced from 263.4 to 30.1 s, and specific resistance to filtration (SRF) falling by 19.6%. Proteins and polysaccharides in tightly bound extracellular polymeric substances (EPS) were also significantly reduced. Based on spectroscopic and electrochemical analysis, we propose mechanisms for the improved dewatering in terms of changes to the sludge's physicochemical properties and EPS. Under strong oxidation, the structure surrounding the bound water is oxidized and bound water is released, so the dewaterability of the sludge is improved.Weiliang Pan and Jiaoni Li contributed equally to this work.

Investigation of the adsorption behavior of Pb(II) onto natural-aged microplastics as affected by salt ions.

In this study, the adsorption behavior of Pb(II) on natural-aged and virgin microplastics in different electrolyte solutions was investigated. The results demonstrated that natural-aged microplastics exhibited higher adsorption capacity for Pb(II) compared to virgin ones, and the addition of CaCl2 strongly inhibited the adsorption amount of Pb(II). The adsorption kinetics of Pb(II) adsorption were better fitted by the pseudo-second order model and Elovich equation, and were slowed down greatly at higher ionic strength. The rate-limiting steps of adsorption process were dominated by intra-particle diffusion. The adsorption isotherm of Pb(II) onto microplastics affected by salt ions can be well described by Freundlich model, the greater adsorption efficiency of natural-aged microplastics proved that adsorption process was multilayer and heterogeneous. In addition, pH significantly influenced the adsorption of Pb(II) due to the changes electrostatic interactions. The effect of fulvic acid in the electrolyte solutions was also revealed and attributed to the complexation with Na+ and Ca2+. Furthermore, the higher pH and ionic strength in different environmental water dramatically decreased adsorption capacity onto microplastics. Finally, it's confirmed that the adsorption mechanisms affected by salt ions mainly involve electrostatic interaction, surface complexation, and ionic exchange. These findings indicate that salt ions exert an important influence on the adsorption of heavy metals for MPs, which should be further concerned.

Microplastics as a vehicle of heavy metals in aquatic environments: A review of adsorption factors, mechanisms, and biological effects.

Microplastics (MPs) have recently attracted much attention due to their widespread distribution in the aquatic environment. Microplastics can act as a vector of heavy metals in the aquatic environment, causing a potential threat to aquatic organisms and human health. This review mainly summarized the occurrence of microplastics in the aquatic environment and their interaction with heavy metals. Then, we considered the adsorption mechanisms of MPs and heavy metals, and further critically discussed the effects of microplastics properties and environmental factors (e.g., pH, DOM, and salinity) on the adsorption of heavy metals. Finally, the potential risks of combined exposure of MPs and heavy metals to aquatic biota were briefly evaluated. This work aims to provide a theoretical summary of the interaction between MPs and heavy metals, and is expected to serve as a reference for the accurate assessment of their potential risks in future studies.

Risk Factors and a Nomogram Model Establishment for Postoperative Delirium in Elderly Patients Undergoing Arthroplasty Surgery: A Single-Center Retrospective Study.

OBJECTIVE: To explore the related risk factors of postoperative delirium (POD) after hip or knee arthroplasty in elderly orthopedic patients and the predictive value of related risk factors. Material and Methods. In total, 309 patients (≥60 years) who received knee and hip arthroplasty between January 2017 and May 2020 were consecutively selected into the POD and nonpostoperative delirium (NPOD) groups. Group bias was eliminated through propensity score matching. Univariate and multivariable logistic analysis was used to determine the risk factors for POD. The nomogram was made by R. RESULTS: 58 patients were included in each group after propensity score matching; multivariable analysis demonstrated that LDH (OR = 4.364, P = 0.017), CHE (OR = 4.640, P = 0.004), Cystatin C (OR = 5.283, P = 0.006), arrhythmia (OR = 5.253, P = 0.002), and operation duration (OR = 1.017, P = 0.050) were independent risk factors of POD. LDH, CHE, Cystatin C, and arrhythmia were used to construct a nomogram to predict the POD. The nomogram was well calibrated and had moderate discriminative ability (AUC = 0.821, 95% CI: 0.760~0.883). Decision curve analysis demonstrated that the nomogram was clinically useful. CONCLUSIONS: Our study revealed that arrhythmia, operation duration, the increase of lactate dehydrogenase and Cystatin C, and the decrease of cholinesterase were reliable factors for predicting postoperative delirium after elderly hip and knee arthroplasty. Meanwhile, the nomogram we developed can assist the clinician to filtrate potential patients with postoperative delirium.

Muscarinic-dependent phosphorylation of the cardiac ryanodine receptor by protein kinase G is mediated by PI3K-AKT-nNOS signaling.

Post-translational modifications of proteins involved in calcium handling in myocytes, such as the cardiac ryanodine receptor (RyR2), critically regulate cardiac contractility. Recent studies have suggested that phosphorylation of RyR2 by protein kinase G (PKG) might contribute to the cardioprotective effects of cholinergic stimulation. However, the specific mechanisms underlying these effects remain unclear. Here, using murine ventricular myocytes, immunoblotting, proximity ligation as-says, and nitric oxide imaging, we report that phosphorylation of Ser-2808 in RyR2 induced by the muscarinic receptor agonist carbachol is mediated by a signaling axis comprising phosphoinositide 3-phosphate kinase, Akt Ser/Thr kinase, nitric oxide synthase 1, nitric oxide, soluble guanylate cyclase, cyclic GMP (cGMP), and PKG. We found that this signaling pathway is compartmentalized in myocytes, as it was distinct from atrial natriuretic peptide receptor-cGMP-PKG-RyR2 Ser-2808 signaling and independent of muscarinic-induced phosphorylation of Ser-239 in vasodilator-stimulated phosphoprotein. These results provide detailed insights into muscarinic-induced PKG signaling and the mediators that regulate cardiac RyR2 phosphorylation critical for cardiovascular function.

Increased RyR2 activity is exacerbated by calcium leak-induced mitochondrial ROS.

Cardiac disease is associated with deleterious emission of mitochondrial reactive oxygen species (mito-ROS), as well as enhanced oxidation and activity of the sarcoplasmic reticulum (SR) Ca2+ release channel, the ryanodine receptor (RyR2). The transfer of Ca2+ from the SR via RyR2 to mitochondria is thought to play a key role in matching increased metabolic demand during stress. In this study, we investigated whether augmented RyR2 activity results in self-imposed exacerbation of SR Ca2+ leak, via altered SR-mitochondrial Ca2+ transfer and elevated mito-ROS emission. Fluorescent indicators and spatially restricted genetic ROS probes revealed that both pharmacologically and genetically enhanced RyR2 activity, in ventricular myocytes from rats and catecholaminergic polymorphic ventricular tachycardia (CPVT) mice, respectively, resulted in increased ROS emission under ß-adrenergic stimulation. Expression of mitochondrial Ca2+ probe mtRCamp1h revealed diminished net mitochondrial [Ca2+] with enhanced SR Ca2+ leak, accompanied by depolarization of the mitochondrial matrix. While this may serve as a protective mechanism to prevent mitochondrial Ca2+ overload, protection is not complete and enhanced mito-ROS emission resulted in oxidation of RyR2, further amplifying proarrhythmic SR Ca2+ release. Importantly, the effects of augmented RyR2 activity could be attenuated by mitochondrial ROS scavenging, and experiments with dominant-negative paralogs of the mitochondrial Ca2+ uniporter (MCU) supported the hypothesis that SR-mitochondria Ca2+ transfer is essential for the increase in mito-ROS. We conclude that in a process whereby leak begets leak, augmented RyR2 activity modulates mitochondrial Ca2+ handling, promoting mito-ROS emission and driving further channel activity in a proarrhythmic feedback cycle in the diseased heart.

Interleukin-1 causes CNS inflammatory cytokine expression via endothelia-microglia bi-cellular signaling.

As a major producer of the inflammatory cytokine interleukin-1 (IL-1), peripheral macrophages can augment IL-1 expression via type 1 IL-1 receptor (IL-1R1) mediated autocrine self-amplification. In the CNS, microglial cells are the major producers of inflammatory cytokines, but express negligible levels of IL-1R1. In the present study, we showed CNS IL-1 induced microglial proinflammatory cytokine expression was mediated by endothelial, not microglial, IL-1R1. This paracrine mechanism was further dissected in vitro. IL-1 was unable to stimulate inflammatory cytokine expression directly from the microglial cell line BV-2, but it stimulated the brain endothelial cell line bEnd.3 to produce a factor(s) in the culture supernatant, which was capable of inducing inflammatory cytokine expression in BV-2. We termed this factor IL-1-induced microglial activation factors (IMAF). BV-2 cytokine expression was inducible by extracellular ATP, but IL-1 did not stimulate the release of ATP from bEnd.3 cells. Filtration of IMAF by size-exclusion membranes showed IMAF activity resided in molecules larger than 50 kd and incubation of IMAF at 95 °C for 5 min did not alter its activity. Microglial inhibitor minocycline was unable to block IMAF activity, even though it blocked LPS induced cytokine expression in BV-2 cells. Adding NF-κB inhibitor to the bEnd.3 cells abolished IL-1 induced cytokine expression in this bi-cellular system, but adding NF-κB inhibitor after IMAF is already produced failed to abrogate IMAF induced cytokine expression in BV-2 cells. RNA sequencing of IL-1 stimulated endothelial cells revealed increased expression of genes involved in the production and processing of hyaluronic acid (HA), suggesting HA as a candidate of IMAF. Inhibition of hyaluronidase by ascorbyl palmitate (AP) abolished IMAF-induced cytokine expression in BV-2 cells. AP administration in vivo also inhibited ICV IL-1-induced IL-1 expression in the hippocampus and hypothalamus. In vitro, either TLR2 or TLR4 inhibitors blocked IMAF induced BV-2 cytokine expression. In vivo, however, IL-1 induced cytokine expression persisted in either TLR2 or TLR4 knockouts. These results demonstrate IL-1 induced inflammatory cytokine expression in the CNS requires a bi-cellular system and HA could be a candidate for IMAF.