A new strategy to stabilize the heavy metals in carbonized MSWI-fly ash using an acid-resistant oligomeric dithiocarbamate chelator.

Fly ash (FA) derived from municipal solid waste incineration (MSWI) requires safe handling before landfilling due to its extremely high salt content and the risk of leaching heavy metals (HMs) under acidic conditions. Herein, aimed at improving the acid stability of dithiocarbamates, a cost-effective oligomeric dithiocarbamate (ODTC) was developed to stabilize HMs from carbonated MSWI-FA. Spiking of 3.6 wt% ODTC reduced the HM leaching below landfill standards in China, even across the pH range of 2.0-13.0 or 8-week exposure to the natural environment. Stabilization decreased the acid-soluble/exchangeable fractions of Cd, Pb, and Zn from 22.2%, 4.49%, and 21.9% to 0.14%, 0.11%, and 12.2%, respectively, resulting in safe levels for Pb and Cd with risk assessments. Compared to DDTC and SDD, ODTC exhibited higher stability under acidic conditions after chelation with the HMs, minimized the risk of HM leaching, and significantly reduced stabilization costs. In-depth studies proved that the stabilization mechanism involved the ability of ODTC to chelate HMs strongly and form acid-resistant ODTC-HM complexes, agglomeration of the MSWI-FA grains to encapsulate the ODTC-HM complexes, transformations of the HMs from acid-soluble species to stable oxidizable and residual species, and specifically ODTC reducing high-valent Pb to more stable Pb(II) species.

The SOX4/EZH2/SLC7A11 signaling axis mediates ferroptosis in calcium oxalate crystal deposition-induced kidney injury.

Epigenetic regulation is reported to play a significant role in the pathogenesis of various kidney diseases, including renal cell carcinoma, acute kidney injury, renal fibrosis, diabetic nephropathy, and lupus nephritis. However, the role of epigenetic regulation in calcium oxalate (CaOx) crystal deposition-induced kidney injury remains unclear. Our study demonstrated that the upregulation of enhancer of zeste homolog 2 (EZH2)-mediated ferroptosis facilitates CaOx-induced kidney injury. CaOx crystal deposition promoted ferroptosis in vivo and in vitro. Usage of liproxstatin-1 (Lip-1), a ferroptosis inhibitor, mitigated CaOx-induced kidney damage. Single-nucleus RNA-sequencing, RNA-sequencing, immunohistochemical and western blotting analyses revealed that EZH2 was upregulated in kidney stone patients, kidney stone mice, and oxalate-stimulated HK-2 cells. Experiments involving in vivo EZH2 knockout, in vitro EZH2 knockdown, and in vivo GSK-126 (an EZH2 inhibitor) treatment confirmed the protective effects of EZH2 inhibition on kidney injury and ferroptosis. Mechanistically, the results of RNA-sequencing and chromatin immunoprecipitation assays demonstrated that EZH2 regulates ferroptosis by suppressing solute carrier family 7, member 11 (SLC7A11) expression through trimethylation of histone H3 lysine 27 (H3K27me3) modification. Additionally, SOX4 regulated ferroptosis by directly modulating EZH2 expression. Thus, this study demonstrated that SOX4 facilitates ferroptosis in CaOx-induced kidney injury through EZH2/H3K27me3-mediated suppression of SLC7A11.

STAT6 promoting oxalate crystal deposition-induced renal fibrosis by mediating macrophage-to-myofibroblast transition via inhibiting fatty acid oxidation.

OBJECTIVE AND DESIGN: Kidney stones commonly occur with a 50% recurrence rate within 5 years, and can elevate the risk of chronic kidney disease. Macrophage-to-myofibroblast transition (MMT) is a newly discovered mechanism that leads to progressive fibrosis in different forms of kidney disease. In this study, we aimed to investigate the role of MMT in renal fibrosis in glyoxylate-induced kidney stone mice and the mechanism by which signal transducer and activator of transcription 6 (STAT6) regulates MMT. METHODS: We collected non-functioning kidneys from patients with stones, established glyoxylate-induced calcium oxalate stone mice model and treated AS1517499 every other day in the treatment group, and constructed a STAT6-knockout RAW264.7 cell line. We first screened the enrichment pathway of the model by transcriptome sequencing; detected renal injury and fibrosis by hematoxylin eosin staining, Von Kossa staining and Sirius red staining; detected MMT levels by multiplexed immunofluorescence and flow cytometry; and verified the binding site of STAT6 at the PPARα promoter by chromatin immunoprecipitation. Fatty acid oxidation (FAO) and fibrosis-related genes were detected by western blot and real-time quantitative polymerase chain reaction. RESULTS: In this study, we found that FAO was downregulated, macrophages converted to myofibroblasts, and STAT6 expression was elevated in stone patients and glyoxylate-induced kidney stone mice. The promotion of FAO in macrophages attenuated MMT and upregulated fibrosis-related genes induced by calcium oxalate treatment. Further, inhibition of peroxisome proliferator-activated receptor-α (PPARα) eliminated the effect of STAT6 deletion on FAO and fibrosis-associated protein expression. Pharmacological inhibition of STAT6 also prevented the development of renal injury, lipid accumulation, MMT, and renal fibrosis. Mechanistically, STAT6 transcriptionally represses PPARα and FAO through cis-inducible elements located in the promoter region of the gene, thereby promoting MMT and renal fibrosis. CONCLUSIONS: These findings establish a role for STAT6 in kidney stone injury-induced renal fibrosis, and suggest that STAT6 may be a therapeutic target for progressive renal fibrosis in patients with nephrolithiasis.

YAP/ACSL4 Pathway-Mediated Ferroptosis Promotes Renal Fibrosis in the Presence of Kidney Stones.

The potential association between calcium oxalate stones and renal fibrosis has been extensively investigated; however, the underlying mechanisms remain unclear. Ferroptosis is a novel form of cell death characterized by iron-dependent lipid peroxidation and regulated by acyl coenzyme A synthase long-chain family member 4 (ACSL4). Yes-associated protein (YAP), a transcriptional co-activator in the Hippo pathway, promotes ferroptosis by modulating ACSL4 expression. Nevertheless, the involvement of YAP-ACSL4 axis-mediated ferroptosis in calcium oxalate crystal deposition-induced renal fibrosis and its molecular mechanisms have not been elucidated. In this study, we investigated ACSL4 expression and ferroptosis activation in the kidney tissues of patients with calcium oxalate stones and in mice using single-cell sequencing, transcriptome RNA sequencing, immunohistochemical analysis, and Western blot analysis. In vivo and in vitro experiments demonstrated that inhibiting ferroptosis or ACSL4 mitigated calcium oxalate crystal-induced renal fibrosis. Furthermore, YAP expression was elevated in the kidney tissues of patients with calcium oxalate stones and in calcium oxalate crystal-stimulated human renal tubular epithelial cell lines. Mechanistically, in calcium oxalate crystal-stimulated human renal tubular epithelial cell lines, activated YAP translocated to the nucleus and enhanced ACSL4 expression, consequently inducing cellular ferroptosis. Moreover, YAP silencing suppressed ferroptosis by downregulating ACSL4 expression, thereby attenuating calcium oxalate crystal-induced renal fibrosis. Conclusively, our findings suggest that YAP-ACSL4-mediated ferroptosis represents an important mechanism underlying the induction of renal fibrosis by calcium oxalate crystal deposition. Targeting the YAP-ACSL4 axis and ferroptosis may therefore hold promise as a potential therapeutic approach for preventing renal fibrosis in patients with kidney stones.

Classification and clinical significance of the posterior group of renal calyces.

To study the anatomical orientation of the posterior group of calyces based on reconstructed images of computerized tomography urography (CTU) and provide a novel classification with its clinical significance. Clinical data of a total of 1321 patients, who underwent CTU examination in our hospital were retrospectively analyzed. Among these, a total of 2642 3-dimensional reconstructed images of CTU scans were considered in this study. Based on the morphology of the renal calyces and the influence on the establishment of surgical access, the posterior group renal calyces are classified into 3 major types including pot-belly type, classically branched and elongated branched. The classically branched type is further classified into 3 sub-types: a, b and c, based on the association of minor calyces of the posterior group to the major calyces. Type a is derived from 1 group of major calyces only, type b is derived from 2 groups of major calyces simultaneously, and type c is derived from 3 groups of major calyces simultaneously. Statistical findings revealed that all kidneys possess posterior group calyces. The percentage of occurrence of pot-belly type, classically branched and elongated branched is 8.06%, 73.13%, and 18.81%, respectively. The anatomical typing of the classical branching type occurred in 19.36%, 68.17%, and 12.47% for types a, b, and c, respectively. In this study, the posterior group calyces were found to be present across all patients. The posterior group calyces were highest in the classical branching type, of which anatomical typing was highest in type b. The typing of the posterior group of calyces could provide an anatomical basis for percutaneous nephrolithotomy (PCNL) puncture from the posterior group.

Overexpression of sirtuin 1 attenuates calcium oxalate-induced kidney injury by promoting macrophage polarization.

Sirtuin 1 (SIRT1) protein is involved in macrophage differentiation, while NOTCH signaling affects inflammation and macrophage polarization. Inflammation and macrophage infiltration are typical processes that accompany kidney stone formation. However, the role and mechanism of SIRT1 in renal tubular epithelial cell injury caused by calcium oxalate (CaOx) deposition and the relationship between SIRT1 and the NOTCH signaling pathway in this urological disorder are unclear. This study investigated whether SIRT1 promotes macrophage polarization to inhibit CaOx crystal deposition and reduce renal tubular epithelial cell injury. Public single-cell sequencing data, RT-qPCR, immunostaining approaches, and Western blotting showed decreased SIRT1 expression in macrophages treated with CaOx or exposed to kidney stones. Macrophages overexpressing SIRT1 differentiated towards the anti-inflammatory M2 phenotype, significantly inhibiting apoptosis and alleviating injury in the kidneys of mice with hyperoxaluria. Conversely, decreased SIRT1 expression in CaOx-treated macrophages triggered Notch signaling pathway activation, promoting macrophage polarization towards the pro-inflammatory M1 phenotype. Our results suggest that SIRT1 promotes macrophage polarization towards the M2 phenotype by repressing the NOTCH signaling pathway, which reduces CaOx crystal deposition, apoptosis, and damage in the kidney. Therefore, we propose SIRT1 as a potential target for preventing disease progression in patients with kidney stones.

p53 deacetylation alleviates calcium oxalate deposition-induced renal fibrosis by inhibiting ferroptosis.

Calcium oxalate (CaOx) stones are among the most common types of kidney stones and are associated with renal tubular damage, interstitial fibrosis, and chronic kidney disease. The mechanism of CaOx crystal-induced renal fibrosis remains unknown. Ferroptosis, a type of regulated cell death, is characterised by iron-dependent lipid peroxidation, and the tumour suppressor p53 is a key regulator of ferroptosis. In the present study, our results demonstrated that ferroptosis was significantly activated in patients with nephrolithiasis and hyperoxaluric mice as well as verified the protective effects of ferroptosis inhibition on CaOx crystal-induced renal fibrosis. Moreover, the single-cell sequencing database, RNA-sequencing, and western blot analysis revealed that the expression of p53 was increased in patients with chronic kidney disease and the oxalate-stimulated human renal tubular epithelial cell line, HK-2. Additionally, the acetylation of p53 was enhanced by oxalate stimulation in HK-2 cells. Mechanistically, we found that the induction of p53 deacetylation, owing to either the SRT1720-induced activation of deacetylase sirtuin 1 or the triple mutation of p53, inhibited ferroptosis and alleviated renal fibrosis caused by CaOx crystals. We conclude that ferroptosis is one of the critical mechanisms contributing to CaOx crystal-induced renal fibrosis, and the pharmacological induction of ferroptosis via sirtuin 1-mediated p53 deacetylation may be a potential target for preventing renal fibrosis in patients with nephrolithiasis.

Gut microbiota in patients with kidney stones: a systematic review and meta-analysis.

BACKGROUND: Mounting evidence indicates that the gut microbiome (GMB) plays an essential role in kidney stone (KS) formation. In this study, we conducted a systematic review and meta-analysis to compare the composition of gut microbiota in kidney stone patients and healthy individuals, and further understand the role of gut microbiota in nephrolithiasis. RESULTS: Six databases were searched to find taxonomy-based comparison studies on the GMB until September 2022. Meta-analyses were performed using RevMan 5.3 to estimate the overall relative abundance of gut microbiota in KS patients and healthy subjects. Eight studies were included with 356 nephrolithiasis patients and 347 healthy subjects. The meta-analysis suggested that KS patients had a higher abundance of Bacteroides (35.11% vs 21.25%, Z = 3.56, P = 0.0004) and Escherichia_Shigella (4.39% vs 1.78%, Z = 3.23, P = 0.001), and a lower abundance of Prevotella_9 (8.41% vs 10.65%, Z = 4.49, P < 0.00001). Qualitative analysis revealed that beta-diversity was different between the two groups (P < 0.05); Ten taxa (Bacteroides, Phascolarctobacterium, Faecalibacterium, Flavobacterium, Akkermansia, Lactobacillus, Escherichia coli, Rhodobacter and Gordonia) helped the detection of kidney stones (P < 0.05); Genes or protein families of the GMB involved in oxalate degradation, glycan synthesis, and energy metabolism were altered in patients (P < 0.05). CONCLUSIONS: There is a characteristic gut microbiota dysbiosis in kidney stone patients. Individualized therapies like microbial supplementation, probiotic or synbiotic preparations and adjusted diet patterns based on individual gut microbial characteristics of patients may be more effective in preventing stone formation and recurrence.

Histone H3K27 methyltransferase EZH2 regulates apoptotic and inflammatory responses in sepsis-induced AKI.

Rationale: The role of histone methylation modifications in renal disease, particularly in sepsis-induced acute kidney injury (AKI), remains unclear. This study aims to investigate the potential involvement of the histone methyltransferase zeste homolog 2 (EZH2) in sepsis-induced AKI and its impact on apoptosis and inflammation. Methods: We first examined the expression of EZH2 in the kidney of sepsis-induced AKI (LPS injection) mice and LPS-stimulated tubular epithelial cells. We next constructed the EZH2 knockout mice to further confirm the effects of EZH2 on apoptosis and inflammatory response in AKI. And the inflammatory level of epithelial cells can be reflected by detecting chemokines and the chemotaxis of macrophages. Subsequently, we constructed the EZH2 knocked-down cells again and performed Chromatin Immunoprecipitation sequencing to screen out the target genes regulated by EZH2 and the enrichment pathway. Then we confirmed the EZH2 target gene and its regulatory pathway in vivo and in vitro experiments. Experimental results were finally confirmed using another in vivo model of sepsis-induced AKI (cecal perforation ligation). Results: The study found that EZH2 was upregulated in sepsis-induced AKI and that silencing EZH2 could reduce renal tubular injury by decreasing apoptosis and inflammatory response of tubular epithelial cells. EZH2 knockout mice showed significantly reduced renal inflammation and macrophage infiltration. Chromatin immunoprecipitation sequencing and polymerase chain reaction identified Sox9 as a target of EZH2. EZH2 was found to be enriched on the promoter of Sox9. Silencing EZH2 resulted in a significant increase in the transcriptional level of Sox9 and activation of the Wnt/ß-catenin signaling pathway. The study further reversed the effects of EZH2 silencing by silencing Sox9 or administering the Wnt/ß-catenin inhibitor icg001. It was also found that Sox9 positively regulated the expression of ß-catenin and its downstream pathway-related genes. Finally, the study showed that the EZH2 inhibitor 3-deazaneplanocin A significantly alleviated sepsis-induced AKI. Conclusion: Our results indicate that silencing EZH2 can protect renal function by relieving transcriptional inhibition of Sox9, activating the Wnt/ß-catenin pathway, and attenuating tubular epithelial apoptosis and inflammatory response of the renal interstitium. These results highlight the potential therapeutic value of targeting EZH2 in sepsis-induced AKI.

Polyamide membranes with nanoscale ordered structures for fast permeation and highly selective ion-ion separation.

Fast permeation and effective solute-solute separation provide the opportunities for sustainable water treatment, but they are hindered by ineffective membranes. We present here the construction of a nanofiltration membrane with fast permeation, high rejection, and precise Cl-/SO42- separation by spatial and temporal control of interfacial polymerization via graphitic carbon nitride (g-C3N4). The g-C3N4 nanosheet binds preferentially with piperazine and tiles the water-hexane interface as revealed by molecular dynamics studies, thus lowering the diffusion rate of PIP by one order of magnitude and restricting its diffusion pathways towards the hexane phase. As a result, membranes with nanoscale ordered hollow structure are created. Transport mechanism across the structure is clarified using computational fluid dynamics simulation. Increased surface area, lower thickness, and a hollow ordered structure are identified as the key contributors to the water permeance of 105 L m2·h-1·bar-1 with a Na2SO4 rejection of 99.4% and a Cl-/SO42- selectivity of 130, which is superior to state-of-the-art NF membranes. Our approach for tuning the membrane microstructure enables the development of ultra-permeability and excellent selectivity for ion-ion separation, water purification, desalination, and organics removal.

Effect of transmembrane protein 100 on prostate cancer progression by regulating SCNN1D through the FAK/PI3K/AKT pathway.

The effects of transmembrane (TMEM) proteins in the progression of prostate cancer (PCa) remain unknown. This study aims to explore the functions of TMEM100 in PCa. To explore the expression, regulation, and effects of TMEM100 in PCa, two PCa cell lines and 30 PCa tissue samples with adjacent control tissues were examined. Online databases, immunohistochemistry, immunofluorescence, western blot, flow cytometry, colony formation, wound healing, transwell assays, and xenograft mouse models were used to explore effects of TMEM100 relevant to PCa. TMEM100 expression was shown to decrease in PCa patients, and low TMEM100 expression was associated with tumor stage and metastasis. Overexpression of TMEM100 suppressed PCa progression by inhibiting the FAK/PI3K/AKT signaling pathway. Tumor size was smaller in TMEM100 overexpressing PCa cells in xenograft mice than in control mice. We also found that TMEM100 could regulate SCNN1D by inhibiting FAK/PI3K/AKT signaling in PCa cell lines. Taken together, our findings indicate that TMEM100 is a tumor suppressor that plays a vital role in preventing PCa proliferation, migration, and invasion through inhibition of FAK/PI3K/AKT signaling. These studies suggest that TMEM100 can be used as a predictive biomarker and therapeutic target.

Effect of mobility on collective phase dynamics of nonlocally coupled oscillators with a phase lag.

Nonlocally coupled oscillators with a phase lag self-organize into various patterns, such as global synchronization, the twisted state, and the chimera state. In this paper, we consider nonlocally coupled oscillators that move on a ring by randomly exchanging their positions with the neighbors and investigate the combined effects of phase lag and mobility on the collective phase dynamics. Spanning the whole range of phase lag and mobility, we show that mobility promotes synchronization for an attractive coupling, whereas it destroys coherence for a repulsive coupling. The transition behaviors are discussed in terms of the timescales of synchronization and diffusion of the oscillators. We also find a novel spatiotemporal pattern at the border between coherent and incoherent states.

Optimization of Fracturing Fluid and Retarded Acid for Stimulating Tight Naturally Fractured Bedrock Reservoirs.

In tight naturally fractured bedrock reservoirs, hydrocarbons are typically stored in fractures, where hydraulic fracturing is needed to connect these fractures to the wellbore. The cross-linked gel is used as the fracturing fluid to reduce the fluid leak-off through natural fractures; however, it can cause formation damage due to its high content of residues after breaking. A synthetic polymer is introduced and evaluated that can maintain a high viscosity to minimize the leak-off , while having a low residue content after breaking. To further enhance the conductivity of the created fracture network, acid is applied to etch and roughen the created fracture faces. Because the target reservoir has a complex mineral composition, a three-step coreflood sequence using reservoir rock samples with controlled fracture widths is established to quantify the enhancement of different retarded acids and to reveal the mechanism behind it. The results indicate the synergy effect of reducing the acid concentration and surfactant adsorption on rock surfaces can lead to an obvious enhancement of the fracture permeability after acidizing, while the mud acid or hydrofluoric acid is not suitable for the target reservoir where concentrations of silicates and clays are relatively high.

Exploring the function of factor XIII free B subunit: Interactions with complement factors and a novel approach to identify potential binding partners.

Background: The factor XIII (FXIII)-B subunit has a critical function as a carrier protein to stabilize FXIII-A in plasma and supply it to its main substrate, fibrinogen. However, the function of the excess free FXIII-B circulating in plasma is still elusive. Objectives: In the present study, we explored potential interactions of free FXIII-B with complement factors and searched for novel binding partners. Methods: We tested for cofactor activity in the degradation of complement C3b and C4b and used ELISA- and surface plasmon resonance-based binding assays to investigate interactions between FXIII-B and complement components. We performed immunoprecipitation and mass spectrometry analysis to identify potential binding partners of free FXIII-B in freshly drawn plasma samples. Results: FXIII-B did not exhibit cofactor activity in the degradation of C3b and C4b similar to factor H and C4b-binding protein, nor did it bind to complement factors to a relevant extent. Identification of proteins potentially binding to free FXIII-B revealed high interindividual variation. We confirmed α2-macroglobulin (α2MG) as a candidate, although direct interactions or functional effects remain to be validated. Conclusions: Our study reveals that free FXIII-B has no direct role in regulating the complement system, despite a structural similarity to major complement regulators. Further studies are needed to validate α2MG as a binding partner and explore potential functional consequences of this binding.

Presence of a Novel Anatomical Structure May Cause Bleeding When Using the Calyx Access in Mini-Percutaneous Nephrolithotomy.

Background: Fused renal pyramid (FRP) is a kidney anatomical structure which was first identified by us. The vascular anatomy of FRP exhibits different from that of the normal renal pyramid (NRP), manifested by the distribution of the ectopic interlobar arteries in FRP. In this study, we analyzed the effect of FRPs on bleeding when using calyx access in mini-percutaneous nephrolithotomy (PCNL). Patients and Methods: Overall, 633 patients who underwent ultrasound-guided single-tract mini-PCNL were divided into two groups according to the puncture method used: in group A, puncture was performed through the axial direction of the renal calyx, the line from the apex of the fornix to the center of the neck plane under B-mode ultrasound guidance; and in group B, Doppler ultrasound-guided axillary puncture through calyces corresponding to NRPs when the plane of renal column blood vessels on both sides was selected or calyx puncture through the hypovascular area of the FRPs. Relevant demographic and clinical data were retrospectively analyzed. Results: The two groups exhibited similar baseline characteristics. No significant differences were found in hemoglobin reduction, puncture site, tract size, postoperative creatinine level, or stone-free rate between the two groups (P > 0.05). Blood transfusion and embolization rates in group B were significantly lower than those in group A (P = 0.03 and 0.045, respectively). No differences were found between the two groups in terms of persistent pain, hydrothorax, fever, subcapsular hematoma, and urosepsis (P > 0.05). The overall complication rate was not significantly different between the two groups (P = 0.505). Conclusions: FRP is a non-negligible anatomical structure that may cause hemorrhage when using calyx access. Doppler ultrasound can identify ectopic blood vessels in FRPs to reduce bleeding during calyx access in mini-PCNL procedures.

The Intersection of Acute Kidney Injury and Non-Coding RNAs: Inflammation.

Acute renal injury (AKI) is a complex clinical syndrome, involving a series of pathophysiological processes, in which inflammation plays a key role. Identification and verification of gene signatures associated with inflammatory onset and progression are imperative for understanding the molecular mechanisms involved in AKI pathogenesis. Non-coding RNAs (ncRNAs), involved in epigenetic modifications of inflammatory responses, are associated with the aberrant expression of inflammation-related genes in AKI. However, its regulatory role in gene expression involves precise transcriptional regulation mechanisms which have not been fully elucidated in the complex and volatile inflammatory response of AKI. In this study, we systematically review current research on the intrinsic molecular mechanisms of ncRNAs that regulate the inflammatory response in AKI. We aim to provide potential research directions and strategies for developing ncRNA-targeted gene therapies as an intervention for the inflammatory damage in AKI.

Preparation of hollow-fiber nanofiltration membranes of high performance for effective removal of PFOA and high resistance to BSA fouling.

Nanofiltration (NF) process has become one of the most promising technologies to remove micro-organic combined water pollution. Developing a NF membrane material with efficient separation for perfluorooctanoic acid (PFOA) combined pollution is highly desired, this manuscript targets this unmet need specifically. In this work, hydrophilic SiO2 nanoparticles with various contents blended with carboxylic multiwalled carbon nanotube were used to modify poly (m-phenylene isophthal amide) (SiO2/CMWCNT/PMIA) hollow fiber NF membrane. The modified membrane with 0.1 wt% SiO2 doping exhibits way better fouling resistance with irreversible fouling ratio decreased dramatically from 18.7% to 2.3%, and the recovery rate of water flux increases significantly from 81.2% to 97.7%. The separation experiment results had confirmed that the modified membrane could improve the rejection from 97.2% to 98.6% for perfluorooctanoic acid (PFOA) and its combined pollution with bovine serum albumin (BSA). It is clear that this reported SiO2/CMWCNT/PMIA hollow fiber NF membrane potentially could be applied in water treatment. This research also provides a theoretical basis for efficiently removal of PFOA and its combined pollution by NF membrane.

Study on the Effect of Fracturing Fluid on the Structure and Mechanical Properties of Igneous Rock.

Igneous rock oil and gas reservoirs have great development potential. Hydraulic fracturing is an important means for the development of these reservoirs. In the process of fracturing and increasing production, fracturing fluid is prone to a hydration reaction with clay minerals in igneous rock, and then, the structure and mechanical properties of the igneous rock are changed, affecting increased production. Therefore, it is necessary to establish a systematic water-rock reaction experiment method to understand the influence of fracturing fluid on the structure and mechanical properties of igneous rocks and to optimize the fracturing fluid system of igneous rock reservoirs. In this experiment, four solutions were used: slickwater, guar fracturing fluid, 2% KCl aqueous solution, and 4% KCl aqueous solution. Acoustic testing, porosity and permeability testing, XRD analysis, micro-CT scanning, and displacement experiments were performed. The influence of different fracturing fluids on the structure and mechanical properties of igneous rocks was studied. Igneous rock samples with a permeability of 0.05-0.1 mD and average porosity of 7-14% were used. The results show that all four liquid systems will reduce the permeability, Young's modulus, and brittleness index and increase the porosity and Poisson's ratio of the rock after fracturing. Among them, the permeability damage rate is as high as 37.37%, which may be related to the plugging of pores with solid residues in the gel breaking liquid; CT results show that there are microcracks in the rock, which increase over time, up to 13.54%. The brittleness index decreases. Among the fluids, the influence of slickwater on the rock brittleness index is the smallest, no more than 5%. Guar gum had the greatest effect on the Gel breaking liquid, up to 58%. One of the reasons for the increase in porosity is that adding a clay stabilizer composed of inorganic salts and organic cationic polymers to the slickwater fracturing fluid can effectively reduce the damage caused by the fracturing fluid to the rock during the fracturing process and can reduce the maximum by 50%. This paper can clarify the damage law of fracturing fluid systems to igneous rock reservoirs and provide the theoretical basis for the hydraulic fracturing of igneous rock reservoirs.

High-Temperature-Resistant, Low-Concentration Water-Controlling Composite Cross-Linked Polyacrylamide Weak Gel System Prepared from Oilfield Sewage.

The polyacrylamide weak gel is an effective system to block a high-permeability layer, realize water control, and enhance oil recovery. However, its application is limited by poor temperature resistance and high polymer dosage. In this paper, an inorganic-organic composite cross-linking agent was synthesized by using Cr(III) and phenolic resin. The composite cross-linking agent can cross-link low concentrations of polyacrylamide to obtain a high-temperature-resistant weak gel system in oilfield sewage. By adjusting the ratio of Cr(III), phenolic resin, and polyacrylamide, an optimum formula MF-7 can be obtained according to the gel strength. Results from evaluation experiments show that the strength of MF-7 can reach H grade even at polyacrylamide concentrations as low as 0.3%. The temperature resistance of the weak gel system is up to 100 °C, and no syneresis occurs after 330 h at 95 °C. Scanning electron microscopy (SEM) results show that MF-7 has a three-dimensional network structure with spherical nodes. The spherical node is composed of polyacrylamide, and its structure size is completely matched with the hydrodynamic radius of the used polyacrylamide. When combined with the network structure formed by Cr(III), the dense cross-linking network structure with nodes can greatly improve the strength and thermal stability of the gel system. The higher the molecular weight of the polyacrylamide used, the higher the strength of the gel obtained. Overall, the composite cross-linking agent can synergistically improve the mechanical properties of the gel, and this weak gel system formed by oilfield sewage is more economical and tolerant.

CXCR4 inhibition attenuates calcium oxalate crystal deposition-induced renal fibrosis.

Nephrolithiasis is a highly prevalent urological disease and results in a correspondingly heavy socioeconomic and healthcare burden. Calcium oxalate (CaOx) stones are among the most common types of kidney stones. They are associated with renal tubular damage, interstitial fibrosis and chronic kidney disease (CKD). However, the molecular mechanisms in CaOx crystal deposition-induced renal fibrosis remain unclear. Chemokines and their receptors act a crucial role in the progression of renal fibrosis through inflammatory cell infiltration, autophagy activation, and epithelial-mesenchymal transition (EMT). The current work aims to study the action and mechanism of the C-X-C motif chemokine receptor 4 (CXCR4) in CaOx crystal deposition-induced renal fibrosis. Transcriptome RNA sequencing, qPCR, and immunohistochemistry revealed that the expression of CXCR4 was significantly upregulated in patients with nephrolithiasis and hyperoxaluric mice. Renal injury and fibrosis were significantly suppressed by inhibiting CXCR4 with AMD3100 or siRNA in hyperoxaluric mice and oxalate-stimulated HK-2 cells; EMT, reactive oxygen species (ROS) levels, and autophagy were also suppressed. Bioinformatic analysis revealed that the NF-κB pathway was activated in hyperoxaluric mice. Mechanistically, activation of the NF-κB pathway was suppressed by CXCR4 inhibition in CaOx crystal-induced renal fibrosis; this suppression was significantly aggravated by the NF-κB inhibitor BAY-11-7085. Moreover, inhibition of autophagy attenuated EMT progression in vitro. Our results suggest that CXCR4 inhibition attenuates CaOx crystal deposition-induced renal fibrosis by suppressing autophagy and EMT through the NF-κB pathway. Therefore, CXCR4 is a potential target for preventing renal fibrosis in patients with nephrolithiasis.