Enhanced aerobic granular sludge by thermally-treated dredged sediment in wastewater treatment under low superficial gas velocity.

The positive contributions of carriers to aerobic granulation have been wildly appreciated. In this study, as a way resource utilization, the dredged sediment was thermally-treated to prepared as carriers to promote aerobic granular sludge (AGS) formation and stability. The system was started under low superficial gas velocity (SGV, 0.6 cm/s)for a lower energy consumption. Two sequencing batch reactors (SBR) labeled R1 (no added carriers) and R2 (carriers added), were used in the experiment. R2 had excellent performance of granulation time (shortened nearly 43%). The maximum mean particle size at the maturity stage of AGS in R2 (0.545 mm) was larger compared to R1 (0.296 mm). The sludge settling performance in R2 was better. The reactors exhibited high chemical oxygen demand (COD) and ammonia nitrogen (NH3-N) removal rates. The total phosphorus (TP) removal rate in R2 was higher than R1 (almost 15% higher) on stage II (93-175d). R2 had a higher microbial abundance and dominant bacteria content. The relative abundance of dominant species was mainly affected by the carrier. However, the enrichment of dominant microorganisms and the evolution of subdominant species were more influenced by the increase of SGV. The results indicated that the addition of carriers induced the secretion of extracellular polymeric substances (EPS) by microorganisms and accelerated the rapid formation of initial microbial aggregates. This work provided a low-cost method and condition to enhance aerobic granulation, which may be helpful in optimizing wastewater treatment processes.

The efficacy of adjuvant chemotherapy in patients with different midpoint-radiotherapy Epstein-Barr virus DNA plasma loads.

OBJECTIVES: This study aimed to evaluate the efficacy of adjuvant chemotherapy (AC) in patients with different midpoint-radiotherapy (mid-RT) Epstein-Barr virus (EBV) DNA plasma loads for locoregionally advanced nasopharyngeal carcinoma (NPC), and to provide decision-making regarding the use of AC. MATERIALS AND METHODS: A total of 675 consecutive patients diagnosed with stage III-IVa NPC were enrolled in this study. All patients underwent concurrent chemoradiotherapy (CCRT), either with or without induction chemotherapy or AC, or a combination of both. The primary endpoint of this study was progression-free survival (PFS). RESULTS: Among the 675 enrolled patients, 248 (36.7 %) received AC and 427 (63.3 %) were only observed after CCRT. In total, 149 (22.1 %) patients had detectable mid-RT EBV DNA levels, whereas 526 (77.9 %) had undetectable mid-RT EBV DNA levels. Patients with detectable mid-RT EBV DNA had worse 5-year PFS than those with undetectable mid-RT EBV DNA (74.8 % vs. 81.9 %, P = 0.045). AC group showed significantly better 5-year PFS than observation in patients with detectable mid-RT EBV DNA (82.8 % vs. 66.8 %; HR, 0.480; 95 % CI 0.250-0.919, P = 0.027). Multivariate analyses demonstrated that the treatment methods (AC vs. observation) were independent prognostic factors for PFS (HR, 0.37; 95 % CI 0.19-0.74, P = 0.005). However, in patients with undetectable mid-RT EBV DNA (5-year PFS: HR 0.873, 95 % CI 0.565-1.349, P = 0.52), AC group showed no survival benefit for observation. CONCLUSION: AC could reduce the risk of disease progression compared to observation in patients with detectable mid-RT EBV DNA. Our findings suggest that AC is effective in patients at a high risk of treatment failure.

NEMF-mediated Listerin-independent mitochondrial translational surveillance by E3 ligase Pirh2 and mitochondrial protease ClpXP.

The ribosome-associated protein quality control (RQC) pathway acts as a translational surveillance mechanism to maintain proteostasis. In mammalian cells, the cytoplasmic RQC pathway involves nuclear export mediator factor (NEMF)-dependent recruitment of the E3 ligase Listerin to ubiquitinate ribosome-stalled nascent polypeptides on the lysine residue for degradation. However, the quality control of ribosome-stalled nuclear-encoded mitochondrial nascent polypeptides remains elusive, as these peptides can be partially imported into mitochondria through translocons, restricting accessibility to the lysine by Listerin. Here, we identify a Listerin-independent organelle-specific mitochondrial RQC pathway that acts on NEMF-mediated carboxy-terminal poly-alanine modification. In the pathway, mitochondrial proteins carrying C-end poly-Ala tails are recognized by the cytosolic E3 ligase Pirh2 and the ClpXP protease in the mitochondria, which coordinately clear ribosome-stalled mitochondrial nascent polypeptides. Defects in this elimination pathway result in NEMF-mediated aggregates and mitochondrial integrity failure, thus providing a potential molecular mechanism of the RQC pathway in mitochondrial-associated human diseases.

Exogenous hydrogen sulfide prevents SOD2 degradation to safeguard renal function in diabetic kidney disease.

Diabetic kidney disease (DKD) is a major contributor to chronic kidney disease. Hydrogen sulfide (H2S) serves as an endogenous gaseous signaling molecule capable of safeguarding renal function within the context of DKD. However, the underlying mechanisms need to be elucidated. This study was undertaken to unveil the mechanisms by which H2S counteracts against DKD. Utilizing mice and human renal tubular epithelial (HK-2) cells, we demonstrated a reduction in cystathionine-γ-lyase/H2S levels within renal tissues of db/db mice and in HK-2 cells subjected to hyperglycemic and hyperlipidemic environments. Notably, we observed that sodium hydrosulfide (NaHS) supplementation could serve as an exogenous source of H2S. Exogenous H2S exhibited the capacity to mitigate the accumulation of reactive oxygen species and attenuate the degradation of superoxide dismutase 2 (SOD2) by Lon protease homolog 1 induced by hyperglycemia and hyperlipidemia, thus affording cellular protection against mitochondrial apoptosis. Consequently, NaHS treatment led to decreased serum levels of blood urea nitrogen and serum creatinine, reflecting alleviated renal damage and thereby preserving renal function in db/db mice. Based on these findings, we propose that exogenous H2S exerts a protective role against DKD by inhibiting SOD2 degradation.

Camrelizumab combined with apatinib in patients with first-line platinum-resistant or PD-1 inhibitor resistant recurrent/metastatic nasopharyngeal carcinoma: a single-arm, phase 2 trial.

Immunotherapy combined with antiangiogenic targeted therapy has improved the treatment of certain solid tumors, but effective regimens remain elusive for refractory recurrent/metastatic nasopharyngeal carcinoma (RM-NPC). We conducted a phase 2 trial to evaluate the safety and activity of camrelizumab plus apatinib in platinum-resistant (cohort 1, NCT04547088) and PD-1 inhibitor resistant NPC (cohort 2, NCT04548271). Here we report on the primary outcome of objective response rate (ORR) and secondary endpoints of safety, duration of response, disease control rate, progression-free survival, and overall survival. The primary endpoint of ORR was met for cohort 1 (65%, 95% CI, 49.6-80.4, n = 40) and cohort 2 (34.3%; 95% CI, 17.0-51.8, n = 32). Grade ≥ 3 treatment-related adverse events (TRAE) were reported in 47 (65.3%) of 72 patients. Results of our predefined exploratory investigation of predictive biomarkers show: B cell markers are the most differentially expressed genes in the tumors of responders versus non-responders in cohort 1 and that tertiary lymphoid structure is associated with higher ORR; Angiogenesis gene expression signatures are strongly associated with ORR in cohort 2. Camrelizumab plus apatinib combination effectiveness is associated with high expression of PD-L1, VEGF Receptor 2 and B-cell-related genes signatures. Camrelizumab plus apatinib shows promising efficacy with a measurable safety profile in RM-NPC patients.

Bayesian inference for survival prediction of childhood Leukemia.

BACKGROUND: Childhood Leukemia is the most common type of cancer among children. Nearly 39% of cancer-induced childhood deaths are attributable to Leukemia. Nevertheless, early intervention has long been underdeveloped. Moreover, there are still a group of children succumbing to their cancer due to the cancer care resource disparity. Therefore, it calls for an accurate predictive approach to improve childhood Leukemia survival and mitigate these disparities. Existing survival predictions rely on a single best model, which fails to consider model uncertainties in predictions. Prediction from a single model is brittle, with model uncertainty neglected, and inaccurate prediction could lead to serious ethical and economic consequences. METHODS: To address these challenges, we develop a Bayesian survival model to predict patient-specific survivals by taking model uncertainty into account. Specifically, we first develop a survival model predict time-varying survival probabilities. Second, we place different prior distributions over various model parameters and estimate their posterior distribution with full Bayesian inference. Third, we predict the patient-specific survival probabilities changing with respect to time by considering model uncertainty induced by posterior distribution. RESULTS: Concordance index of the proposed model is 0.93. Moreover, the standardized survival probability of the censored group is higher than that of the deceased group. CONCLUSIONS: Experimental results indicate that the proposed model is robust and accurate in predicting patient-specific survivals. It can also help clinicians track the contribution of multiple clinical attributes, thereby enabling well-informed intervention and timely medical care for childhood Leukemia.

Alpha-kinase1 promotes tubular injury and interstitial inflammation in diabetic nephropathy by canonical pyroptosis pathway.

BACKGROUND: Alpha-kinase 1 (ALPK1) is a master regulator in inflammation and has been proved to promote renal fibrosis by promoting the production of IL-1ß in diabetic nephropathy (DN) mice. Pyroptosis is involved in high glucose (HG)-induced tubular cells injury, characterized by activation of Gasdermin D (GSDMD) and the release of IL-1ß and IL-18, resulting in inflammatory injury in DN. It is reasonable to assume that ALPK1 is involved in pyroptosis-related tubular injury in DN. However, the mechanism remains poorly defined. METHODS: Immunohistochemistry (IHC) staining was performed to detect the expression of pyroptosis- and fibrosis-related proteins in renal sections of DN patients and DN mice. DN models were induced through injection of streptozotocin combined with a high-fat diet. Protein levels of ALPK1, NF-κB, Caspase-1, GSDMD, IL-1ß, IL-18 and α-SMA were detected by Western blot. HK-2 cells treated with high-glucose (HG) served as an in vitro model. ALPK1 small interfering RNA (siRNA) was transfected into HK-2 cells to down-regulate ALPK1. The pyroptosis rates were determined by flow cytometry. The concentrations of IL-1ß and IL-18 were evaluated by ELISA kits. Immunofluorescence staining was used to observe translocation of NF-κB and GSDMD. RESULTS: The heat map of differentially expressed genes showed that ALPK1, Caspase-1 and GSDMD were upregulated in the DN group. The expression levels of ALPK1, Caspase-1, GSDMD and CD68 were increased in renal biopsy tissues of DN patients by IHC. ALPK1expression and CD68+ macrophages were positively correlated with tubular injury in DN patients. Western blot analysis showed increased expressions of ALPK1, phospho-NF-κB P65, GSDMD-NT, and IL-1ß in renal tissues of DN mice and HK-2 cells, accompanied with increased renal fibrosis-related proteins (FN, α-SMA) and macrophages infiltration in interstitial areas. Inhibition of ALPK1 attenuated HG-induced upregulation expressions of NF-κB, pyroptosis-related proteins Caspase-1, GSDMD-NT, IL-1ß, IL-18, α-SMA, and pyroptosis level in HK-2 cells. Also, the intensity and nuclear translocation of NF-κB and membranous translocation of GSDMD were ameliorated in HG-treated HK-2 cells after treatment with ALPK1 siRNA. CONCLUSIONS: Our data suggest that ALPK1/NF-κB pathway initiated canonical caspase-1-GSDMD pyroptosis pathway, resulting in tubular injury and interstitial inflammation of DN.

Insights into the enhanced effect of biochar on cadmium removal in vertical flow constructed wetlands.

Biochar has been increasingly applied in constructed wetlands (CWs) to remediate heavy metal (HM)-polluted water. Nevertheless, only few studies have elucidated the enhanced mechanism and potential synergies related to the HM removal from biochar-based CWs (BC-CWs) for HMs removal. This study used cadmium (Cd) as the target HM and added biochar into CWs to monitor physicochemical parameters, plant' physiological responses, substrate accumulation, and microbial metabolites and taxa. In comparison with the biochar-free CW (as CWC), a maximum Cd2+ removal of 99.7% was achieved in the BC-CWs, associated with stable physicochemical parameters. Biochar preferentially adsorbed the available Cd2+ and significantly accumulated Fe/Mn oxides-bond and the exchangeable Cd fraction. Moreover, biochar alleviated the lipid peroxidation (decreased by 36.4%) of plants, resulting in improved growth. In addition, extracellular polymeric substances were increased by 376.9-396.8 mg/L in BC-CWs than compared to CWC, and N and C cycling was enhanced through interspecific positive connectivity. In summary, this study explored comprehensively the performance and mechanism of BC-CWs in the treatment of Cd2+-polluted water, suggesting a promising approach to promote the plant-microbe-substrate synergies under HM toxicity.

Alpha-kinase1 promotes tubular injury and interstitial inflammation in diabetic nephropathy by canonical pyroptosis pathway

BACKGROUND: Alpha-kinase 1 (ALPK1) is a master regulator in inflammation and has been proved to promote renal fibrosis by promoting the production of IL-1ß in diabetic nephropathy (DN) mice. Pyroptosis is involved in high glucose (HG)-induced tubular cells injury, characterized by activation of Gasdermin D (GSDMD) and the release of IL-1ß and IL-18, resulting in inflammatory injury in DN. It is reasonable to assume that ALPK1 is involved in pyroptosis-related tubular injury in DN. However, the mechanism remains poorly defined. METHODS: Immunohistochemistry (IHC) staining was performed to detect the expression of pyroptosis- and fibrosis-related proteins in renal sections of DN patients and DN mice. DN models were induced through injection of streptozotocin combined with a high-fat diet. Protein levels of ALPK1, NF-κB, Caspase-1, GSDMD, IL-1ß, IL-18 and α-SMA were detected by Western blot. HK-2 cells treated with high-glucose (HG) served as an in vitro model. ALPK1 small interfering RNA (siRNA) was transfected into HK-2 cells to down-regulate ALPK1. The pyroptosis rates were determined by flow cytometry. The concentrations of IL-1ß and IL-18 were evaluated by ELISA kits. Immunofluorescence staining was used to observe translocation of NF-κB and GSDMD. RESULTS: The heat map of differentially expressed genes showed that ALPK1, Caspase-1 and GSDMD were upregulated in the DN group. The expression levels of ALPK1, Caspase-1, GSDMD and CD68 were increased in renal biopsy tissues of DN patients by IHC. ALPK1expression and CD68+ macrophages were positively correlated with tubular injury in DN patients. Western blot analysis showed increased expressions of ALPK1, phospho-NF-κB P65, GSDMD-NT, and IL-1ß in renal tissues of DN mice and HK-2 cells, accompanied with increased renal fibrosis-related proteins (FN, α-SMA) and macrophages infiltration in interstitial areas. Inhibition of ALPK1 attenuated HG-induced upregulation expressions of NF-κB, pyroptosis-related proteins Caspase-1, GSDMD-NT, IL-1ß, IL-18, α-SMA, and pyroptosis level in HK-2 cells. Also, the intensity and nuclear translocation of NF-κB and membranous translocation of GSDMD were ameliorated in HG-treated HK-2 cells after treatment with ALPK1 siRNA. CONCLUSIONS: Our data suggest that ALPK1/NF-κB pathway initiated canonical caspase-1-GSDMD pyroptosis pathway, resulting in tubular injury and interstitial inflammation of DN.

Oxalate crystal-related acute renal injury caused by orlistat: A case report. / å¥¥åˆ©å¸ä»–è‡´è‰é ¸ç›ç»“æ™¶ç›¸å ³æ€¥æ€§è‚¾æŸä¼¤1例.

We reported a case of oxalate crystal-related acute kidney injury caused by orlistat. The patient was admitted for nephrotic syndrome and acute kidney injury. The pathomorphological assessment of renal biopsy showed intratubular oxalate crystals. The patient reported that she had taken orlistat regularly to loss weight for more than a year. This patient had a habit of drinking vegetable soup and strong herbal tea daily. Orlistat, an intestinal lipase inhibitor, may cause secondary hyperoxaluria, that is, intestinal hyperoxaluria. Dietary habits could be a common precipitating factor for orlistat-relevant hyperoxaluria. It was comprehensively considered to be oxalate crystal-related acute renal injury, and the patient's renal function recovered gradually after drug withdrawal. Clinicians should pay attention to screening drug-related acute kidney injury including orlistat when observing patients with unexplained acute kidney injury, and renal biopsy should be performed if necessary. It is also important to warn people who take the orlistat for weight loss about the side effects of this drug so as to adjust the eating habits.

The antibacterial activity of a novel NK-lysin homolog and its molecular characterization and expression in the striped catfish, Pangasianodon hypophthalmus.

Aeromonas hydrophila was a common bacterial pathogen in aquaculture resulting in considerable losses to the striped catfish aquaculture industry. As an emergent antimicrobial peptide (AMP), NK-lysin (NKL) had activity against various microorganisms. However, the antibacterial activity of NKL from striped catfish (Pangasianodon hypophthalmus) both in vitro and vivo remains unclear. In this study, the cDNA sequence of P. hypophthalmus NK-lysin gene (PhNK-lysin) was cloned and characterized. The amino acid sequence of PhNK-lysin contains a signal peptide sequence of 17 amino acid (aa) residues and a mature peptide composed of 130 aa. The saposin B domain of mature peptide comprised six conserved cysteines forming three putative disulfide bonds. Phylogenetic analysis revealed that the PhNK-lysin was most closely related to that of the channel catfish (Ictalurus punctatus) NK-lysin. The transcriptional levels of the PhNK-lysin were significantly upregulated in response to A. hydrophila infection in various tissues including heart, liver, spleen, head kidney, trunk kidney and gill. The synthetic PhNK-lysin-derived peptide consisting of 38aa showed antibacterial activity against Vibrio harveii, Aeromonas hydrophila and Escherichia coli. The MIC for V. harveii, A. hydrophila and E. coli were 15.625 µM, 250 µM and 31.25 µM respectively. Besides, the synthetic PhNK-lysin decreased the bacterial load of liver and trunk kidney in vivo as well as increased the survival rate of A. hydrophila infected striped catfish. Hence, these data suggest that PhNK-lysin had antimicrobial effect and protects the host from pathogenic infection.

A review of enrichment methods for circulating tumor cells: from single modality to hybrid modality.

Circulating tumor cell (CTC) analysis as a liquid biopsy can be used for early diagnosis of cancer, evaluating cancer progression, and assessing treatment efficacy. The enrichment of CTCs from patient blood is important for CTC analysis due to the extreme rarity of CTCs. This paper updates recent advances in CTC enrichment methods. We first review single-modality methods, including biophysical and biochemical methods. Hybrid-modality methods, combining at least two single-modality methods, are gaining increasing popularity for their improved performance. Then this paper reviews hybrid-modality methods, which are categorized into integrated and sequenced hybrid-modality methods. The state of the art indicates that the CTC capture efficiencies of integrated hybrid-modality methods can reach 85% or higher by taking advantage of the superimposed and enhanced capture effects from multiple single-modality methods. Moreover, a hybrid method integrating biophysical with biochemical methods is characterized by both high processing rate and high specificity.

Modeling of pre-transplantation liver viability with spatial-temporal smooth variable selection.

BACKGROUND AND OBJECTIVE: Liver viability assessment plays a critical role in liver transplantation, and the accuracy of the assessment directly determines the success of the transplantation surgery and patient's outcomes. With various factors that affect liver viability, including pre-existing medical conditions of donors, the procurement process, and preservation conditions, liver viability assessment is typically subjective, invasive or inconsistent in results among different surgeons and pathologists. Motivated by these challenges, we aimed to create a non-invasive statistical model utilizing spatial-temporal infrared image (IR) data to predict the binary liver viability (acceptable/unacceptable) during the preservation. METHODS: The spatial-temporal features of liver surface temperature, monitored by IR thermography, are significantly correlated with the liver viability. A spatial-temporal smooth variable selection (STSVS) method is proposed to define the smoothness of model parameters corresponding to different liver surface regions at different times. RESULTS: A case study, using porcine livers, has been performed to validate the efficacy of the STSVS method. The comparison results show that STSVS has the better overall prediction performance compared to the past state-of-the-art predictive models, including generalized linear model (GLM), support vector machine (SVM), LASSO, and Fused LASSO. Moreover, the significant predictors identified by the STSVS method indicate the importance of edges of lobes in predicting liver viability during the pre-transplantation preservation. CONCLUSIONS: The proposed method has the best performance in predicting liver viability. This 'real-time' prediction method may increase the utilization of donors' livers without damaging tissues and time-consuming, yet imprecise feature assessment.

In-depth research on percarbonate expediting zero-valent iron corrosion for conditioning anaerobically digested sludge.

Anaerobically digested sludge (ADS) is commonly hard to dewater for the presence of extracellular polymeric substances (EPS) and the liberation of glutinous soluble microbic products during anaerobic digestion. Sodium percarbonate (SPC) expediting zero-valent iron (ZVI) corrosion (SPC/ZVI) process firstly conditioned ADS to amend its dewaterability. Results showed that SPC/ZVI conditioning decreased moisture content of dewatered cake from 90.5% (control) to 69.9% with addition of 0.10 g/g TS SPC and 0.20 g/g TS ZVI. Mechanistic research indicated that the enhanced ADS dewaterability mainly resulted from •OH and Fe(III)/iron polymers yielded in SPC/ZVI. •OH disrupted EPS, damaged cytoderm & cytomembrane, and lysed intracellular substances, unbinding the bound water. Meanwhile, the breakage and inactivation of microbe by •OH prompted the production of macro-pores in ADS. •OH adjusted the conformation of extracellular/intracellular proteins by intervening in the H-bonds and S-S bonds, availing the hydrophobicity and slight flocculation of ADS. •OH further facilitated the despiralization of α-helical to ß-sheet structure in ADS pellets, benefiting cell-to-cell aggregation. Additionally, Fe(III)/iron polymers from ZVI corrosion accelerated to gather ADS and maintained its floc structure. Consequently, SPC/ZVI conditioning not only adjusted the natures of ADS and its EPS but also the features of residual pellets, which further induced the advancement of ADS dewaterability. In addition, SPC/ZVI conditioning possibly surmounts some limitations existing in ZVI/Peroxide or ZVI/Persulfate technique.

Digestion liquid based alkaline pretreatment of waste activated sludge promotes methane production from anaerobic digestion.

This work proved an efficient method to significantly increase methane production from anaerobic digestion of WAS. This method is to reflux proper of digestion liquid into waste activated sludge pretreatment unit (pH 9.5 for 24 h). The yield of maximum methane improved between 174.2 ± 7.3 and 282.5 ± 14.1 mL/g VSS with the reflux ratio of digestion liquid increasing from 0% to 20%. It was observed that the biodegradable organics in the digestion liquid did not affect the biological processes related to anaerobic digestion but increased methane production through reutilization. The ammonium in the digestion liquid was the main contributor to the increase in methane production via promoting sludge solubilization, but refractory organics were the major inhibitors to anaerobic digestion. It should be emphasized that the metal ions present in the digestion liquid were beneficial rather than harmful to the biological processes in the anaerobic digestion, which may be connected with the fact that certain metal ions were involved in the expression and activation of key enzymes. In addition, it was found that anaerobes in digestion liquid were another potential contributor to the enhanced anaerobic digestion.

Peroxide/Zero-valent iron (Fe0) pretreatment for promoting dewaterability of anaerobically digested sludge: A mechanistic study.

Peroxide/Zero-valent iron (Fe0) was reported to promote dewaterability of anaerobically digested sludge (ADS), but the mechanism of how Peroxide/Fe0 facilitates ADS dewatering is unknown. This study therefore aims to uncover the details of how Peroxide/Fe° elevates ADS dewaterability. Experimental results showed that with 0.6 g Fe0/g TSS and 0.08 g peroxide/g TSS, capillary suction time, specific resistance to filtration, and time to filtration of ADS was 50.7 %, 41.4 %, and 54.4 % of that in the control, respectively. In this condition, water content of sludge cake decreased from 91.2 % ± 0.5 % (the control) to 68.6 % ± 1.3 %. The mechanism explorations revealed that the elevated dewaterability was mainly caused by role of OH and Fe(II)/Fe(III) species during Peroxide/Fe° pretreatment. OH decreased the polysaccharides and proteins in extracellular polymeric substance (EPS), then injured the cytoderm & cytomembrane through the releases of lactate dehydrogenase and N-acetylglucosamine, and further facilitated the decrease of intracellular substances, which disengaged the water trapped in ADS. In addition, the cell lysis caused by OH facilitated forming macro-pores. Moreover, OH converted the conformational structure of extracellular proteins, which may strengthen the ADS hydrophobicity, promoting the discharge of unbound water and ADS flocculation. Meanwhile, Fe(II)/Fe(III) benefited aggregating the denatured ADS particulates.

Norfloxacin-induced effect on enhanced biological phosphorus removal from wastewater after long-term exposure.

In this study, long-term experiments were performed under synthetic wastewater conditions to evaluated the potential impacts of norfloxacin (NOR) (10, 100 and 500 µg/L) on enhanced biological phosphorus removal (EBPR). Experimental result showed that long-term exposure to 10 µg/L NOR induced negligible effects on phosphorus removal. The presence of 100 µg/L NOR slightly decreased phosphorus removal efficiency to 94.41 ± 1.59 %. However, when NOR level further increased to 500 µg/L, phosphorus removal efficiency was significantly decreased from 97.96 ± 0.8 5% (control) to 82.33 ± 3.07 %. The mechanism study revealed that the presence of 500 µg/L NOR inhibited anaerobic phosphorus release and acetate uptake as well as aerobic phosphorus uptake during long-term exposure. It was also found that 500 µg/L NOR exposure suppressed the activity of key enzymes related to phosphorus removal but promoted the transformations of intracellular polyhydroxyalkanoate and glycogen. Microbial analysis revealed that that the presence of 500 µg/L NOR reduced the abundances of polyphosphate accumulating organisms but increased glycogen accumulating organisms, as compared the control.

Fe(II) catalyzing sodium percarbonate facilitates the dewaterability of waste activated sludge: Performance, mechanism, and implication.

In this work, Fe(II) catalyzing sodium percarbonate (Fe(II)/SPC) was managed to facilitate waste activated sludge (WAS) dewatering for the first time. The results showed that after WAS was treated by 20 mg/g total suspended solids (TSS) Fe(II) and 50 mg/g TSS SPC, the water content of sludge cake (WCSC) by press filtration and capillary suction time (CST) dropped from 90.8% ± 1.6% and 96.1 ± 4.0 s (the control) to 55.6% ± 1.4% and 30.1 ± 2.5 s, respectively. The mechanism investigations indicated that four intermediates or products (i.e., •OH, H2O2, Fe(II), and Fe(III)) generated in the Fe(II)/SPC process were responsible for the improved WAS dewaterability, and •OH and Fe(III) were the two major contributors. It was found that •OH collapsed and fragmented extracellular polymeric substances, damaged cell wall and permeabilized cytoplasmic membrane, and transformed conformation of the extracellular proteins secondary structure via both affecting the hydrogen bond maintaining α-helix and cracking disulfide bond in cysteine residues while Fe(III), the oxidization product of Fe(II), decreased the surface electronegativity and water-affinity surface areas of WAS flocs. As a result, the bound water release, flocculability, surface hydrophobicity, drain capability, and flowability of WAS flocs were strengthened whereas the compact surface structure, colloidal forces, network strength, gel-like structure, and apparent viscosity of WAS flocs were weakened. In addition, Fe(II)/SPC process also reduced the recalcitrant organics and fecal coliforms in sludge, which facilitated land application of dewatered sludge. The findings acquired in this work not only deepens our understanding of Fe(II)/SPC-involved WAS treatment process but also may guide engineers to develop both effective and promising strategies to better condition WAS for dewatering in the future.

New insight into modification of extracellular polymeric substances extracted from waste activated sludge by homogeneous Fe(II)/persulfate process.

Fe(II)/persulfate process has been proven to be a promising technique for disintegrating sludge, while during the Fe(II)/persulfate treatment the direct information about the variation of extracellular polymeric substances (EPS) properties, which is a key factor affecting sludge dewatering, is still lacked. In this work, different dosages of Fe(II)/persulfate were employed to treat EPS fractions extracted from waste activated sludge. The experiment results showed that EPS fractions were modified by Fe(II)/persulfate process. An oxidation/flocculation process was raised to unveil how Fe(II)/persulfate modified EPS fractions: Firstly, SO4- and OH were formed by chemical reactions of Fe(II) activating persulfate and radical interconversion, respectively. Then these species nonselectively fragmented EPS fractions through decomposing their components, which facilitated decrement of the hydrophilic components and high/mid molecular weight of organics in EPS fractions. Furthermore, these radicals transformed the secondary structure of EPS proteins by affecting the hydrogen bonds at specific positions and inducing the cleavage of the S-S bonds in cysteine residues of proteins, which led to loose layout of protein molecules and thus increased exposure of the hydrophobic groups hidden in EPS protein molecules. Secondly, Fe(III), i.e., the oxidation product of Fe(II), assembled the ruptured colloids particles through lessening electronegativity. Consequently, Fe(II)/persulfate process elevated the flocculability and hydrophobicity of EPS fractions, which would improve physicochemical and rheological properties of sludge to facilitate its dewaterability.

Rosiglitazone Suppresses Calcium Oxalate Crystal Binding and Oxalate-Induced Oxidative Stress in Renal Epithelial Cells by Promoting PPAR-γ Activation and Subsequent Regulation of TGF-ß1 and HGF Expression.

Peroxisome proliferator-activated receptor- (PPAR-) γ is a ligand-dependent transcription factor, and it has become evident that PPAR-γ agonists have renoprotective effects, but their influence and mechanism during the development of calcium oxalate (CaOx) nephrolithiasis remain unknown. Rosiglitazone (RSG) was used as a representative PPAR-γ agonist in our experiments. The expression of transforming growth factor-ß1 (TGF-ß1), hepatocyte growth factor (HGF), c-Met, p-Met, PPAR-γ, p-PPAR-γ (Ser112), Smad2, Smad3, pSmad2/3, and Smad7 was examined in oxalate-treated Madin-Darby canine kidney (MDCK) cells and a stone-forming rat model. A CCK-8 assay was used to evaluate the effects of RSG on cell viability. In addition, intracellular reactive oxygen species (ROS) levels were monitored, and lipid peroxidation in renal tissue was detected according to superoxide dismutase and malondialdehyde levels. Moreover, the location and extent of CaOx crystal deposition were evaluated by Pizzolato staining. Our results showed that, both in vitro and in vivo, oxalate impaired PPAR-γ expression and phosphorylation, and then accumulative ROS production was observed, accompanied by enhanced TGF-ß1 and reduced HGF. These phenomena could be reversed by the addition of RSG. RSG also promoted cell viability and proliferation and decreased oxidative stress damage and CaOx crystal deposition. However, these protective effects of RSG were abrogated by the PPAR-γ-specific inhibitor GW9662. Our results revealed that the reduction of PPAR-γ activity played a critical role in oxalate-induced ROS damage and CaOx stone formation. RSG can regulate TGF-ß1 and HGF/c-Met through PPAR-γ to exert antioxidant effects against hyperoxaluria and alleviate crystal deposition. Therefore, PPAR-γ agonists may be expected to be a novel therapy for nephrolithiasis, and this effect is related to PPAR-γ-dependent suppression of oxidative stress.