Intestinal CXCR6+ ILC3s migrate to the kidney and exacerbate renal fibrosis via IL-23 receptor signaling enhanced by PD-1 expression.

Group 3 innate lymphoid cells (ILC3s) regulate inflammation and tissue repair at mucosal sites, but whether these functions pertain to other tissues-like the kidneys-remains unclear. Here, we observed that renal fibrosis in humans was associated with increased ILC3s in the kidneys and blood. In mice, we showed that CXCR6+ ILC3s rapidly migrated from the intestinal mucosa and accumulated in the kidney via CXCL16 released from the injured tubules. Within the fibrotic kidney, ILC3s increased the expression of programmed cell death-1 (PD-1) and subsequent IL-17A production to directly activate myofibroblasts and fibrotic niche formation. ILC3 expression of PD-1 inhibited IL-23R endocytosis and consequently amplified the JAK2/STAT3/RORγt/IL-17A pathway that was essential for the pro-fibrogenic effect of ILC3s. Thus, we reveal a hitherto unrecognized migration pathway of ILC3s from the intestine to the kidney and the PD-1-dependent function of ILC3s in promoting renal fibrosis.

Asymmetric Electrode Design for High-Area Capacity and High-Energy Efficiency Hybrid Zn Batteries.

Compared to Zn-air batteries, by integrating Zn-transition metal compound reactions and oxygen redox reactions at the cell level, hybrid Zn batteries are proposed to achieve higher energy density and energy efficiency. However, attaining relatively higher energy efficiency relies on controlling the discharge capacity. At high area capacities, the proportion of the high voltage section can be neglected, resulting in a lower energy efficiency similar to that of Zn-air batteries. Here, a high-loading integrated electrode with an asymmetric structure and asymmetric wettability is fabricated, which consists of a thick nickel hydroxide (Ni(OH)2) electrode layer with vertical array channels achieving high capacity and high utilization, and a thin NiCo2O4 nanopartical-decorated N-doped graphene nanosheets (NiCo2O4/N-G) catalyst layer with superior oxygen catalytic activity. The asymmetric wettability satisfies the wettability requirements for both Zn-Ni and Zn-air reactions. The hybrid Zn battery with the integrated electrode exhibits a remarkable peak power density of 141.9 mW cm-2, superior rate performance with an energy efficiency of 71.4% even at 20 mA cm-2, and exceptional cycling stability maintaining a stable energy efficiency of ≈84% at 2 mA cm-2 over 100 cycles (400 h).

Corticosteroid in IgA nephropathy with moderate proteinuria: A retrospective cohort study.

BACKGROUND: Corticosteroids remain contentious as a therapeutic option for IgA nephropathy. We conducted a retrospective cohort study to explore whether corticosteroid therapy is efficient and safe for IgAN patients with moderate proteinuria. METHODS: A total of 336 patients with renal biopsy-confirmed IgAN, estimated glomerular filtration (eGFR) over 15 mL/min/1.73 m2 and urine protein levels of 0.75-3.5 g/d were enrolled. According to the treatment protocol, we classified the enrolled patients into two groups: one receiving corticosteroids and the other receiving supportive care. Complete remission, partial remission, and no remission were applied to describe the efficacy assessments. The endpoint was defined as a 40% reduction in eGFR, the onset of ESRD, or renal disease-related death. RESULTS: Clinical and pathological progression risk factors were higher in corticosteroid-treated individuals. Logistic regression analysis revealed that the corticosteroid group was considerably related to a higher remission rate after adjustment for confounding factors. The occurrence of serious adverse events between the two groups was not found to be statistically significantly different. Then, we matched 95 couples of patients with similar baseline levels in both groups by propensity score matching. The results showed that corticosteroid-treated patients showed higher overall and complete remission rates than untreated patients. However, due to the relatively short follow-up period, no significant differences in the incidence of endpoint and survival analyses have been observed thus far. CONCLUSION: Corticosteroid therapy may benefit IgAN patients with moderate proteinuria via proteinuria reduction and renal function preservation.

Left ventricular strain and myocardial work in short-term peritoneal dialysis patients.

BACKGROUND: Initiation of dialysis encompasses new cardiovascular challenges on patients with end-stage renal disease (ESRD). This study used two-dimensional speckle-tracking echocardiography (2D-STE) to investigate the change of left ventricular (LV) myocardial function undergoing peritoneal dialysis (PD) within 1-3 months. METHODS: A total of 56 patients with ESRD and 27 healthy controls were enrolled in this prospective study. Mean duration of PD was 44.41 ± 16.44 days. We evaluated LV myocardial function of patients with ESRD in baseline and within 1-3 months after PD by 2D-STE with global longitudinal strains (GLS) and myocardial work (MW). Based on the level of serum phosphate before PD, patients were divided into two groups: the group with normal serum phosphate or hyperphosphatemia. RESULTS: Compared with healthy controls, patients with ESRD had impaired GLS (p < .001) and increased global work index (GWI) (p = .034), global constructive work (GCW) (p < .001), global wasted work (GWW) (p < .001), and lower global work efficiency (GWE) (p = .002). After PD therapy, GWI (p = .001), GCW (p < .001), and GWW (p = .023) decreased and closed to healthy subjects (p > .05) and no significant improvement was observed in GLS (p = .387). GLS of basal segments worsened in the hyperphosphatemia group (p = .005) and GWW reduced remarkably in the group with normal serum phosphate after PD treatment (p = .008). The change of left ventricular internal diameter in diastole (LVIDd) was the only parameter influenced GWI in post-dialysis patients (ß = 0.324, p = .013). CONCLUSIONS: Short-term PD treatment improved LV MW in ESRD patients. They benefited more when receiving treatment before the increase of serum phosphorus.

Comparative analysis between the safety and efficacy of oral corticosteroids versus corticosteroids pulse therapies in IgA nephropathy.

OBJECTIVE: This study retrospectively compared the safety and efficacy of oral corticosteroid therapy (OCT) and corticosteroid pulse therapy (CPT) in the treatment of IgA nephropathy. METHODS: One ninety-two patients were diagnosed with IgA nephropathy and had an estimated glomerular filtration rate > 15mL/min/1.73m2 and 24-h urine protein level of 0.75-3.5g. Patients were divided into CPT and OCT groups according to the treatment protocol. The differences in the efficacy and safety between the two groups were assessed by logistic regression analysis and propensity score matching. RESULTS: Significant differences at baseline, including 24-h urine protein level and eGFR, were observed between the two groups. Logistic regression analysis indicated that the remission rate increased significantly, while the incidences of total adverse events and infections decreased in CPT group compared with the OCT group after adjusting the potential confounding factors. Forty-seven pairs of subjects are matched by using propensity score matching with similar baseline data. The results indicate that the total remission rate and complete remission rate were significantly higher, while the incidences of total adverse events were lower (p = 0.008) in the CPT group than in the OCT group. The subgroup analysis showed that CPT group was more likely to achieve remission in patients with initial 24-h urine protein levels falling into the range of 2-3.5 g and Oxford Classification of S1 or C1/2 (p < 0.05). CONCLUSION: Among patients with IgA nephropathy and 24-h urine protein levels of 0.75-3.5g, CPT may be more effective than OCT in reducing urinary protein levels and improving renal function with a lower incidence of adverse events.

Arid2-IR promotes NF-κB-mediated renal inflammation by targeting NLRC5 transcription.

Increasing evidence shows that long non-coding RNAs (lncRNAs) play an important role in a variety of disorders including kidney diseases. It is well recognized that inflammation is the initial step of kidney injury and is largely mediated by nuclear factor Kappa B (NF-κB) signaling. We had previously identified lncRNA-Arid2-IR is an inflammatory lncRNA associated with NF-κB-mediated renal injury. In this study, we examined the regulatory mechanism through which Arid2-IR activates NF-κB signaling. We found that Arid2-IR was differentially expressed in response to various kidney injuries and was induced by transforming growth factor beta 1(TGF-ß1). Using RNA sequencing and luciferase assays, we found that Arid2-IR regulated the activity of NF-κB signal via NLRC5-dependent mechanism. Arid2-IR masked the promoter motifs of NLRC5 to inhibit its transcription. In addition, during inflammatory response, Filamin A (Flna) was increased and functioned to trap Arid2-IR in cytoplasm, thereby preventing its nuclear translocation and inhibition of NLRC5 transcription. Thus, lncRNA Arid2-IR mediates NF-κB-driven renal inflammation via a NLRC5-dependent mechanism and targeting Arid2-IR may be a novel therapeutic strategy for inflammatory diseases in general.

Effect of Mean Platelet Volume to Platelet Count Ratio on Mortality in Peritoneal Dialysis.

Background and Aims: Mean platelet volume to platelet count ratio (MPV/PC) has been found to be an independent risk factor for mortality in various diseases, including cardiovascular disease, cancer, and hemodialysis. We aimed to evaluate the association between MPV/PC and all-cause and cardiovascular (CV) mortality in peritoneal dialysis (PD) patients. Methods and Results: We conducted a retrospective cohort study at a single center and enrolled 1473 PD patients who were catheterized at our PD center from January 1, 2006, to December 31, 2013. All patients were divided into four groups according to the quartiles of baseline MPV/PC levels and followed up until December 31, 2018. A total of 453 patients died, and 221 deaths were caused by cardiovascular disease during a median follow-up time of 48.0 (21.9-82.2) months. There was a significant interaction by age of association between MPV/PC level and all-cause mortality (P = 0.009), and multivariate Cox regression analysis showed that higher MPV/PC level was related to a decreased risk of all-cause and CV mortality in PD patients aged < 60 years (HR = 0.62, 95%CI = 0.40 - 0.96, P = 0.032; HR = 0.49, 95%CI = 0.26 - 0.93, P = 0.029, respectively), rather than in patients aged ≥ 60 years (HR = 1.37, 95%CI = 0.84 - 2.22, P = 0.208; HR = 1.50, 95%CI = 0.77 - 2.92, P = 0.237, respectively). Conclusion: Our results indicated that low MPV/PC level was an independent risk factor for all-cause and CV mortality in PD patients aged less than 60 years.

Identification of Smad3-related transcriptomes in type-2 diabetic nephropathy by whole transcriptome RNA sequencing.

Smad3 deficiency prevents the development of type 2 diabetic nephropathy; however, the underlying molecular mechanisms remain unknown. In this study, we aimed to identify Smad3-related genes involved in the pathogenesis of diabetic kidney disease. High-throughput RNA sequencing was performed to profile the whole transcriptome in the diabetic kidney of Smad3 WT-db/db, Smad3 KO-db/db, Smad3+/- db/db and their littermate control db/m mice at 20 weeks. The gene ontology, pathways and alternative splicing of differentially expressed protein-coding genes and long non-coding RNAs related to Smad3 in diabetic kidney were analysed. Compared to Smad3 WT-db/db mice, Smad3 KO-db/db mice exhibited an alteration of genes associated with RNA splicing and metabolism, whereas heterozygosity deletion of Smad3 (Smad3+/- db/db mice) significantly altered genes related to cell division and cell cycle. Notably, three protein-coding genes (Upk1b, Psca and Gdf15) and two lncRNAs (NONMMUG023520.2 and NONMMUG032975.2) were identified to be Smad3-dependent and to be associated with the development of diabetic nephropathy. By using whole transcriptome RNA sequencing, we identified novel Smad3 transcripts related to the development of diabetic nephropathy. Thus, targeting these transcripts may represent a novel and effective therapy for diabetic nephropathy.

Identification of differentially expressed circulating exosomal lncRNAs in IgA nephropathy patients.

BACKGROUND: Although immunoglobulin A nephropathy (IgAN) is one of the foremost primary glomerular disease, treatment of IgAN is still in infancy. Non-invasive biomarkers are urgently needed for IgAN diagnosis. We investigate the difference in expression profiles of exosomal long non-coding-RNAs (lncRNAs) in plasma from IgAN patients compared with their healthy first-degree relatives, which may reveal novel non-invasive IgAN biomarkers. METHODS: We isolated exosomes from the plasma of both IgAN patients and their healthy first-degree relatives. High-throughput RNA sequencing and real-time quantitative polymerase chain reaction (qRT-PCR) was used to validate lncRNA expression profiles. Pathway enrichment analysis was used to predict their nearest protein-coding genes. RESULTS: lncRNA-G21551 was significantly down-regulated in IgAN patients. Interestingly, the nearest protein-coding gene of lncRNA-G21551 was found to be encoding the low affinity receptor of the Fc segment of immunoglobulin G (FCGR3B). CONCLUSIONS: Exosomal lncRNA-G21551, with FCGR3B as the nearest protein-coding gene, was down-regulated in IgAN patients, indicating its potential to serve as a non-invasive biomarker for IgAN.

Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs.

BACKGROUND: Though the roles of microRNAs (miRNAs) in renal diseases have been extensively investigated, a thorough screening and comparison of miRNAs among different types of chronic kidney disease (CKD) has never been performed. METHODS: The intrarenal miRNAs were profiled from fresh kidney tissues of patients with biopsy-proven minimal change disease (MCD), focal segmental glomerular sclerosis (FSGS) and diabetic nephropathy (DN) by using microarray. Commonly dysregulated miRNAs were validated by real-time PCR using paraffin-embedded renal tissues from all three types of CKD patients as well as mouse unilateral ureteral obstruction (UUO) model. Two novel miRNAs were selected and annotations of their target genes were performed using GO and KEGG pathway enrichment analysis. Biological functions of three two candidate miRNAs were explored in TGF-ß1-induced cell model using human kidney proximal tubular cells (HK-2). RESULTS: The kidney biopsy samples of three disease types represent different levels of damage and fibrosis, which were the mildest in MCD, moderate in FSGS, and the most severe in DN. 116 miRNAs were identified to be commonly dysregulated, including 40 up-regulated and 76 down-regulated in CKD tissues as compared with healthy donor kidney biopsy tissues. Two novel miRNAs, hsa-miR-3607-3p and hsa-miR-4709-3p, were verified as consistently differentially expressed among all three types of patient samples as well as in mouse model. In vitro, hsa-miR-3607-3p was repressed while hsa-miR-4709-3p was induced by TGF-ß1 treatment. Inhibition of hsa-miR-3607-3p or overexpression of hsa-miR-4709-3p promoted TGF-ß1-induced migration and F-actin assembling in HK-2 cells, which are characteristics of epithelial-mesenchymal transition (EMT). Further study identified that ITGB8 and CALM3 were the bona fide target genes of hsa-miR-3607-3p and hsa-miR-4709-3p respectively. CONCLUSIONS: The present identify a unique miRNAs profile that probably relates to the common fibrosis process of CKD. Results of our study suggest that hsa-miR-3607-3p and hsa-miR-4709-3p may represent as promising therapeutic targets against kidney fibrosis.

Finite element analysis of the effect of power arm locations on tooth movement in extraction space closure with miniscrew anchorage in customized lingual orthodontic treatment.

INTRODUCTION: More patients are choosing customized orthodontic appliances because of their excellent esthetics. It is essential that clinicians understand the biomechanics of the tooth movement tendency in customized lingual orthodontics. This study aimed to evaluate the tooth movement tendency during space closure in maxillary anterior teeth with the use of miniscrew anchorage in customized lingual orthodontics with various power arm locations. METHODS: Three-dimensional finite element models of the maxilla were created with miniscrews and power arms; the positions were varied to change the force directions. A retraction force (1.5 N) was applied from the top of the miniscrews to the selected points on the power arm, and the initial displacements of the reference nodes of the maxillary teeth were analyzed. RESULTS: After applying force in different directions, power arms located at the distal side of the canines led to larger initial lingual crown tipping and occlusal crown extrusion of the maxillary incisors compared with power arms located at the midpoint between the lateral incisors and canines, and caused a decreasing trend of the intercanine width. CONCLUSIONS: In customized lingual orthodontic treatment, power arms located at the distal side of the canines are unfavorable for anterior teeth torque control and intercanine width control. Power arms located at the midpoint between the lateral incisors and canines can get better torque control, but still cannot achieve excepted torque without extra torque control methods, no matter whether its force application point is higher than, lower than, or equal to the level of the top of the miniscrews.

Prognostic value of inflammation-based prognostic scores on outcome in patients undergoing continuous ambulatory peritoneal dialysis.

BACKGROUND: Inflammation-based prognostic scores have been used as outcome predictors in patients with cancer or on hemodialysis. However, their role in patients on continuous ambulatory peritoneal dialysis (CAPD) remains unclear. This study aimed to examine the prognostic value of inflammation-based composite scores for mortality in CAPD patients. METHODS: This study was conducted in CAPD patients enrolled from January 1, 2006 to December 31, 2014 and followed until December 31, 2016. Three inflammation-based prognostic scores, including Glasgow prognostic score (GPS), prognostic nutritional index (PNI), and prognostic index (PI), were conducted in this study. The associations between these scores and all-cause or cardiovascular mortality were evaluated by Kaplan-Meier method and Cox proportional hazards models. The areas under the curve (AUC) of receiver-operating characteristic (ROC) analysis were used to determine the predictive values of mortality. RESULTS: A total of 1501 patients were included. During a median follow-up of 38.7 (range, 21.6-62.3) months, 346 (23.1%) patients died, of which 168 (48.6%) were due to cardiovascular diseases (CVD). After adjustment for confounders, the results showed that elevated GPS, PNI, and PI scores were all independently associated with all-cause [GPS: Score 1: hazard ratio(HR) 3.94, 95% confidence interval(CI) 2.90-5.35; Score 2: HR 7.56, 95% CI 5.35-10.67; PNI: HR 1.82, 95% CI 1.36-2.43; PI: Score 1: HR 2.08, 95% CI 1.63-2.65; Score 2: HR 3.03, 95% CI 2.00-4.60)] and CVD mortality(GPS: Score 1: HR 4.41, 95% CI 2.76-7.03; Score 2: HR 9.64, 95% CI 5.72-16.26; PNI: HR 1.63, 95% CI 1.06-2.51; PI: Score 1: HR 2.57, 95% CI 1.81-3.66, Score 2: HR 3.85, 95% CI 1.99-7.46).The AUC values of GPS score were 0.798 (95% CI0.770-0.826) for all-cause mortality and 0.781 (95% CI 0.744-0.817) for CVD mortality, both of which significantly higher than those of PNI and PI scores (P < 0.001, respectively). CONCLUSIONS: All elevated GPS, PNI, and PI scores were independently associated with all-cause and CVD mortality. The GPS score showed better predictive value than PNI and PI scores in CAPD patients.

An intelligent detection method for high-field asymmetric waveform ion mobility spectrometry.

In conventional high-field asymmetric waveform ion mobility spectrometry signal acquisition, multi-cycle detection is time consuming and limits somewhat the technique's scope for rapid field detection. In this study, a novel intelligent detection approach has been developed in which a threshold was set on the relative error of α parameters, which can eliminate unnecessary time spent on detection. In this method, two full-spectrum scans were made in advance to obtain the estimated compensation voltage at different dispersion voltages, resulting in a narrowing down of the whole scan area to just the peak area(s) of interest. This intelligent detection method can reduce the detection time to 5-10% of that of the original full-spectrum scan in a single cycle.

Long Noncoding RNA Arid2-IR Is a Novel Therapeutic Target for Renal Inflammation.

Increasing evidence shows that microRNAs play an important role in kidney disease. However, functions of long noncoding RNAs (lncRNAs) in kidney diseases remain undefined. We have previously shown that TGF-ß1 plays a diverse role in renal inflammation and fibrosis and Smad3 is a key mediator in this process. In this study, we used RNA-sequencing to identify lncRNAs related to renal inflammation and fibrosis in obstructive nephropathy induced in Smad3 wild-type and knockout mice. We found that Arid2-IR was a Smad3-associated lncRNA as a Smad3 binding site was found in the promoter region of Arid2-IR and deletion of Smad3 abolished upregulation of Arid2-IR in the diseased kidney. In vitro knockdown of Arid2-IR from tubular epithelial cells produced no effect on TGF-ß-induced Smad3 signaling and fibrosis but inhibited interleukin-1ß-stimulated NF-κB-dependent inflammatory response. In contrast, overexpression of Arid2-IR promoted interleukin-1ß-induced NF-κB signaling and inflammatory cytokine expression without alteration of TGF-ß1-induced fibrotic response. Furthermore, treatment of obstructed kidney with Arid2-IR shRNA blunted NF-κB-driven renal inflammation without effect on TGF-ß/Smad3-mediated renal fibrosis. Thus, Arid2-IR is a novel lncRNA that functions to promote NF-κB-dependent renal inflammation. Blockade of Arid2-IR may represent a novel and specific therapy for renal inflammatory disease.

Opposing roles for Smad2 and Smad3 in peritoneal fibrosis in vivo and in vitro.

Peritoneal fibrosis is a major cause of ultrafiltration failure in patients receiving continuous ambulatory peritoneal dialysis. Transforming growth factor (TGF)-ß1 is an important mediator in this process; however, its signaling mechanisms had not been explored. Thus, we examined TGF-ß1/Smad signaling in human peritoneal biopsy specimens associated with continuous ambulatory peritoneal dialysis. We found that TGF-ß/Smad2/3 signaling was highly activated in patients with increased collagen deposition and thickening of the peritoneal membrane who were receiving continuous ambulatory peritoneal dialysis. Long-term exposure of wild-type mice to 4.25% peritoneal dialysis solution for 30 days induced significant peritoneal fibrosis with impaired peritoneal equilibrium, which was prevented in Smad3 knockout mice. In contrast, conditional Smad2 gene deletion in the peritoneum exacerbated peritoneal fibrosis and dysfunction. The contrasting roles of Smad2 and Smad3 in peritoneal fibrosis were also examined in vitro. Cultured mesothelial cells from Smad3 knockout mice were resistant to TGF-ß1-induced collagen I production and the transition toward a myofibroblast phenotype as seen in wild-type cells, whereas Smad2 deficiency in mesothelial cells failed to modulate the profibrotic response to TGF-ß1. In conclusion, this study found activation of TGF-ß/Smad signaling in peritoneal fibrosis in patients receiving continuous ambulatory peritoneal dialysis and identifies opposing roles for Smad2 and Smad3 in peritoneal dialysis-associated peritoneal fibrosis. These findings provide a mechanistic basis for future therapies targeting TGF-ß/Smad signaling in peritoneal fibrosis.

MicroRNA-29b inhibits peritoneal fibrosis in a mouse model of peritoneal dialysis.

TGF-ß/Smad3 signaling plays a pivotal role in the pathogenesis of peritoneal fibrosis associated with peritoneal dialysis (PD). MicroRNA-29 (miR-29) is known as a potent downstream inhibitor of TGF-ß/Smad3 in renal fibrosis. In this study, we examined the therapeutic potential for miR-29b on PD-related peritoneal fibrosis in a mouse model of PD induced by daily infusion of 4.25% dextrose-containing PD fluid (PDF). MiR-29b-expressing plasmid was delivered into the peritoneum via an ultrasound-microbubble-mediated system before and at day 14 after PDF. We found that mice on PD developed peritoneal fibrosis with impaired peritoneal function, which was associated with a loss of miR-29b. In contrast, overexpression of miR-29b before the PDF infusion showed a protective effect on peritoneal fibrosis including EMT and prevented peritoneal dysfunction. Moreover, delayed miR-29b treatment until peritoneal fibrosis was established at day 14 also halted the progression of peritoneal fibrosis at day 28. Further studies identified that blockade of the Sp1-TGF-ß/Smad3 pathway may be a mechanism by which miR-29b inhibited peritoneal fibrosis. In conclusion, treatment with miR-29b may represent a novel and effective therapy for PD-associated peritoneal fibrosis.

Fluidized Reduction Kinetics of Boron-Bearing Iron Concentrate by Hydrogen at Low Temperatures Based on Model-Fitting and Model-Free Methods.

Pyrometallurgy is the most effective way to comprehensively utilize boron-bearing iron concentrate, and there is an urgency for an environmentally friendly and efficient method to achieve the prereduction of boron-bearing iron concentrate. In this study, the mechanism and kinetics of isothermal hydrogen reduction of boron-bearing iron concentrate in a fluidized bed at 500-570 °C were discussed. The reduction degree was quantified in combination with the online gas composition analysis technique, and the phase and microstructure of the reduced products were characterized. The results exhibited that the apparent activation energy remained constant during the whole reduction process, with average values of 50.67 and 48.08 kJ/mol calculated by the model-free and model-fitting methods, respectively, and the reaction was controlled by the contracting sphere model. The formation of a microporous metallic iron facilitated the rapid penetration of hydrogen to the reaction interface. Therefore, the intrinsic chemical reaction at the interface determined the whole reaction process.

Design of Thick Electrodes with Vertical Channels for Aqueous Batteries: Experimental and Numerical Analysis.

Developing thick electrodes with high-area loadings is a direct method for boosting the energy density. However, this approach also leads to a proportional increase in the resistance to charge transport. Optimizing the microstructure of the electrode can effectively enhance the charge transport kinetics in thick electrodes. Herein, a low-tortuosity nickel electrode with vertical channels (VC-Ni) is fabricated using a phase inversion method. A high-loading VC-Ni electrode (26.7 mg cm-2) delivers a superior specific capacity of 134.0 mAh g-1 at a 5 C rate, significantly outperforming the conventional nickel electrode (Con-Ni). Numerical simulations reveal the fast transport kinetics within the vertical channel electrodes. For the thick electrode, the VC-Ni electrode shows a substantially lower concentration gradient of OH- and H+ compared to the Con-Ni electrode. Notably, beyond a critical loading of 26.5 mg cm-2, the specific capacity initially increases with volume fraction, peaking at 50%, and then diminishes. The specific capacity increases as the channel size decreases, but the tendency to increase gradually decreases. The highest specific capacity is achieved with an inverted trapezoidal channel shape, characterized by larger pores near the separator and smaller pores near the current collector. This work is of guidance for the design of thick electrodes for high-performance aqueous batteries.

Re-examination of the genotoxic activity of water taken from the Songhua River in P. R. China.

The Songhua River, in northeast China, has heavy organic contamination due to domestic sewage and industrial wastewater. Thus, it is important to further determine its genotoxic activity, which is a potential hazard for human health. Short-term genotoxic bioassays using Salmonella, the cytokinesis-block micronucleus cytome assay, and mouse liver cell comet assay were employed to further examine the genotoxic activity of diethyl ether extracts of water samples taken from the Songhua River. Ames test results showed that there were still frame-shift mutagens, both direct and indirect, in water samples at doses of 5.0 or 7.0 L water equivalent/plate. The mutagenicity seems to be less when compared with the results from 2002 to 2003. A dose-response relationship was also obtained between DNA damage in mouse liver cells by comet assay and micronuclei formation by CBMN assay. These results indicate that the water samples showed genotoxic activity with a mutagenic potency. 88 and 104 compounds, respectively, were identified in summer and winter water sample extracts by gas chromatography-mass spectrometry analysis. Four priority pollutants listed by the United States Environmental Protection Agency and six priority pollutants listed by the Chinese Environment Protection Agency were found in summer or winter water samples, respectively. The results indicate that the diethyl ether extracts of surface water samples taken from the Songhua River still show genotoxic activity (≥3.0 L water). The risks of potential carcinogenicity for human health in the Songhua River should be studied further.

Tailoring the Electrochemical Deposition of Zn by Tuning the Viscosity of the Liquid Electrolyte.

The issues during Zn deposition in rechargeable Zn-based batteries greatly hinder cycling stability. In this work, a simple and inexpensive approach to tailor the Zn electrodeposition is proposed by tuning the viscosity of the liquid electrolyte (LE). First, the growth mechanisms of Zn deposition under different electrolyte properties are investigated by numerical simulation, from which the bottom deposition tends to fuse with each other when there are more deposition sites, and the mass-transfer coefficient is lower, thus achieving uniform deposition. Besides, the whole process of Zn deposition in charging-discharging cycling is in situ observed by an optical microscope. It is found that the cause of the poor stability in the LE is due to the uneven Zn deposition, resulting in weak bonding between the deposition and the electrode surface, which is also the reason for the formation of dead Zn. In contrast, when an appropriate amount of the polymer is added to the LE to increase the viscosity, an appropriate overpotential can be created, generating more deposition sites. In addition, the viscosity reduces the mass-transfer coefficient, making the distance from the ion to the deposition sites the main controlling factor. The Zn ions are more inclined to move in the direction of electric field lines, which results in a uniform and dense deposition layer. Furthermore, the effectiveness of this method is demonstrated in a Zn-LiFePO4 battery, from which the battery with the modified electrolyte condition still works properly even in the Zn utilization of 100% and shows a capacity retention rate (35%) of nearly twice that in the original LE condition (18%) after 10 cycles. This work provides a theoretical basis for Zn deposition and provides ideas for the future development of high-performance Zn-based batteries.