Dityrosine-inspired photocrosslinking technique for 3D printing of silk fibroin-based composite hydrogel scaffolds.

Photoinduced self-crosslinking technology is a great facilitator of 3D bioprinting of silk fibroin (SF) by allowing rapid solidification of a deliberately formulated SF-based photocrosslinkable bioink. An SF-based, photocrosslinked hydrogel was fabricated with tyramine-modified sodium carboxymethyl cellulose (CMC-Na) as a co-crosslinkable constituent and Ru(bpy)3Cl2 (Ru(II)) and potassium persulfate (KPS) as blue light photoinitiators. Photorheological studies demonstrated that the photocrosslinking and viscoelasticity of the composite could be tuned by varying the relative content of the two constituents. Xanthan gum (XG) was employed in formulating the SF-based photocrosslinkable bioink, and the improved rheological properties and printability were evidenced by the resulting tunable shear-thinning behavior and shear thixotropy. 3D SF-based hydrogel scaffolds with uniform pores with a size of approximately 550 µm × 1000 µm were constructed via extrusion-based printing and a simple 30 s post-photocrosslinking combined process. Furthermore, the CMC-Na incorporated 3D hydrogel scaffolds exhibited sufficient structural strength, adequate filament fineness, and tunable transparency, which shows a promising prospect in the application of tissue engineering and regenerative medicine.

Risk factors for hypocalcemia in dialysis patients with refractory secondary hyperparathyroidism after parathyroidectomy: a meta-analysis.

OBJECTIVE: Hypocalcemia after parathyroidectomy (PTX) results in tetany, diarrhea, cardiac arrhythmia, and even sudden death. However, a meta-analysis or systematic evaluation of risk factors with the occurrence and development of hypocalcemia in patients with secondary hyperparathyroidism (SHPT) after PTX has never been performed. METHODS: A thorough search of electronic databases, including PubMed, Web of Science, the Cochrane Library, and EMBASE, was performed to retrieve relevant studies from database inception to June 2021. Quality of the included studies was assessed by two independent reviewers using the Newcastle-Ottawa Scale. Review Manager 5.3 and Stata 16.0 were used for meta-analysis. The random-effects model was adopted to calculate the 95% CIs (I2> 50% or p < 0.05) of the combined effect size and the corresponding homogeneous data. Otherwise, a fixed-effects model was used. RESULTS: Thirteen studies including 2990 participants who met the inclusion criteria were enrolled in the present meta-analysis. The overall quality of the enrolled studies had a score of >7 points. Risk factors significantly related to hypocalcemia in patients with SHPT after PTX were preoperative serum calcium (OR 0.19, 95%CI 0.11-0.31), preoperative alkaline phosphatase (ALP) (OR 1.01, 95% CI 1.01-1.02), and preoperative intact parathyroid hormone (iPTH) (OR 1.38, 95%CI 1.20-1.58). Meanwhile, age (OR 0.97, 95%CI 0.87-1.10) was not significantly correlated with hypocalcemia after PTX. CONCLUSIONS: Based on the current evidence, preoperative serum calcium, preoperative ALP, and preoperative iPTH were significant predictors of hypocalcemia in patients with SHPT after PTX. More attention should be given to patients with these risk factors for the prevention of postoperative hypocalcemia.

Blue Light Induced Photopolymerization and Cross-Linking Kinetics of Poly(acrylamide) Hydrogels.

Blue light induced photopolymerization and photo-cross-linking kinetics of acrylamide (AM), with camphorquinone/diphenyl iodonium hexafluorophosphate (CQ/DPI) as photoinitiators, were investigated. The effects of a number of parameters, including mass fraction of CQ, DPI, and AM (wCQ, wDPI, and wAM) and light intensity (I), on photopolymerization efficiency and photogelation process were systematically studied by photo-differential scanning calorimetry (DSC) and photo-rheometry. Photo-DSC indicated that the maximum photopolymerization rate (Rp, max) was proportional to wCQ0.5, wDPI0.5, I0.5, and wAM, while Photo-Rheometry showed linear relationships between gel time tgel and wCQ and I, respectively, and power law relationships between tgel and wDPI and wAM, respectively. In addition, both peak cross-linking rate Rc,max, and delay time td, which were both linearly proportional to wCQ0.5, wDPI0.5, and I0.5, showed power law relationships with wAM. Furthermore, exponential patterns were observed between all these factors, wCQ, wDPI, wAM, and I and plateau modulus G'∞. Combining such correlations obtained from experimental data, an empirical model was established describing the projected mechanical properties of poly(acrylamide) hydrogels from blue light initiated photopolymerization and photo-cross-linking.

Interleukin-13 promotes expression of Alix to compromise renal tubular epithelial barrier function.

The epithelial barrier dysfunction plays a critical role in a number of kidney diseases. The mechanism is unclear. Alix is a protein involving in protein degradation in epithelial cells. This study aims to investigate that interleukin (IL)-13 inhibits Alix to compromise the kidney epithelial barrier function. In this study, the murine collecting duct cell line (M-1) was cultured in Transwell inserts to investigate the significance of Alix in compromising the epithelial barrier functions. T cell (Teff cells) proliferation assay was employed to assess the antigenicity of ovalbumin (OVA) that was transported across the M-1 monolayer barrier. The results showed that M-1 cells express Alix. Exposure to interleukin (IL)-13 markedly decreased the expression of Alix in M-1 cells, which compromised the M-1 monolayer barrier functions by showing the increases in the permeability to OVA. Over-expression of Alix abolished the IL-13-induced M-1 monolayer barrier dysfunction. Knockdown of Alix significantly increased M-1 monolayer permeability. The OVA collected from the Transwell basal chambers induced the OVA-specific T cell proliferation. We conclude that IL-13 compromises M-1 epithelial barrier functions via inhibiting Alix expression.

Biodegradation of dichlorodiphenyltrichloroethanes (DDTs) and hexachlorocyclohexanes (HCHs) with plant and nutrients and their effects on the microbial ecological kinetics.

Four pilot-scale test mesocosms were conducted for the remediation of organochlorine pesticides (OCPs)-contaminated aged soil. The results indicate that the effects on degradation of hexachlorocyclohexanes (HCHs) and dichlorodiphenyltrichloroethanes (DDTs) were in the following order: nutrients/plant bioaugmentation (81.18 % for HCHs; 85.4 % for DDTs) > nutrients bioaugmentation > plant bioaugmentation > only adding water > control, and nutrients/plant bioaugmentation greatly enhanced the degradation of HCHs (81.18 %) and DDTs (85.4 %). The bacterial community structure, diversity and composition were assessed by 454-pyrosequencing of 16S recombinant RNA (rRNA), whereas the abundance of linA gene was determined by quantitative polymerase chain reaction. Distinct differences in bacterial community composition, structure, and diversity were a function of remediation procedure. Predictability of HCH/DDT degradation in soils was also investigated. A positive correlation between linA gene abundance and the removal ratio of HCHs was indicated by correlation analyses. A similar relationship was also confirmed between the degradation of HCHs/DDTs and the abundance of some assemblages (Gammaproteobacteria and Flavobacteria). Our results offer microbial ecological insight into the degradation of HCHs and DDTs in aged contaminated soil, which is helpful for the intensification of bioremediation through modifying plant-microbe patterns, and cessation of costly and time-consuming assays.

Microbial community dynamics of soil mesocosms using Orychophragmus violaceus combined with Rhodococcus ruber Em1 for bioremediation of highly PAH-contaminated soil.

Understanding of the effects of perturbation strategies on soil microorganisms is helpful in optimizing bioremediation systems and enhancing their efficiency. Four soil mesocosms were constructed for bioremediation of highly polycyclic aromatic hydrocarbon-contaminated soil using the flowering plant Orychophragmus violaceus and/or bacterium Rhodococcus ruber Em1. Bacterial community dynamics were evaluated by 454 pyrosequencing, and Em1 abundance was assessed by quantitative polymerase chain reaction. The results showed that the diversity of the bacterial community increased gradually with time; the degree of increase was in the order mesocosm PE (combination of O. violaceus and Em1), mesocosm WE (Em1), mesocosm PC (O. violaceus only), mesocosm WA (attenuation). Increased diversity may be predictive of PAH degradation. O. violaceus had a marked effect on bacterial community evolution and promoted the growth of Em1. The bacterial community of mesocosm PE gradually separated from the others, as indicated by Venn diagrams and weight-principal component analysis. Abundances of the families Cytophagaceae + Nocardioidaceae + Iamiacaeae (Actinobacteria), and Alcanivoracaceae + Pseodomonadaceae + Xanthomonadaceae (Gammaproteobacteria) were positively correlated with PAH degradation. Our findings help bridge the gap between field bioremediation and laboratory approaches, provide insight into processes of microbial ecological recovery, and will be useful in developing strategies to optimize bioremediation by modifying plant-microbe interaction patterns.

Involvement of p300/CBP and epigenetic histone acetylation in TGF-ß1-mediated gene transcription in mesangial cells.

Transforming growth factor-ß1 (TGF-ß1)-induced expression of plasminogen activator inhibitor-1 (PAI-1) and p21 in renal mesangial cells (MCs) plays a major role in glomerulosclerosis and hypertrophy, key events in the pathogenesis of diabetic nephropathy. However, the involvement of histone acetyl transferases (HATs) and histone deacetylases (HDACs) that regulate epigenetic histone lysine acetylation, and their interaction with TGF-ß1-responsive transcription factors, are not clear. We evaluated the roles of histone acetylation, specific HATs, and HDACs in TGF-ß1-induced gene expression in rat mesangial cells (RMCs) and in glomeruli from diabetic mice. Overexpression of HATs CREB binding protein (CBP) or p300, but not p300/CBP-activating factor, significantly enhanced TGF-ß1-induced PAI-1 and p21 mRNA levels as well as transactivation of their promoters in RMCs. Conversely, they were significantly attenuated by HAT domain mutants of CBP and p300 or overexpression of HDAC-1 and HDAC-5. Chromatin immunoprecipitation assays showed that TGF-ß1 treatment led to a time-dependent enrichment of histone H3-lysine9/14-acetylation (H3K9/14Ac) and p300/CBP occupancies around Smad and Sp1 binding sites at the PAI-1 and p21 promoters. TGF-ß1 also enhanced the interaction of p300 with Smad2/3 and Sp1 and increased Smad2/3 acetylation. High glucose-treated RMCs exhibited increased PAI-1 and p21 levels, and promoter H3K9/14Ac, which were blocked by TGF-ß1 antibodies. Furthermore, increased PAI-1 and p21 expression was associated with elevated promoter H3K9/14Ac levels in glomeruli from diabetic mice. Thus TGF-ß1-induced PAI-1 and p21 expression involves interaction of p300/CBP with Smads and Sp1, and increased promoter access via p300/CBP-induced H3K9/14Ac. This in turn can augment glomerular dysfunction linked to diabetic nephropathy.

Effect of prolonged tacrolimus treatment in idiopathic membranous nephropathy with nephrotic syndrome.

OBJECTIVE: Tacrolimus has been used for idiopathic membranous nephropathy (IMN) therapy, but most patients who achieved remission showed a high relapse rate when tacrolimus was withdrawn after 6-12 months of therapy. We proposed that a prolonged therapeutic course should help reduce the relapse rate. METHODS: A total of 42 patients with nephrotic syndrome caused by IMN were randomly divided into short-term (n = 20) and long-term (n = 22) groups. All patients received initial treatment with tacrolimus and prednisone for 6 months, and afterward only the long-term patient group was tapered with low-dose tacrolimus until 24 months. RESULTS: Over 85% of the patients achieved proteinuria reduction, serum albumin improvement and serum lipid recovery; the probability of remission in both groups was over 80% at 6 months. The remission rate was steady at over 80% after 12 and 24 months in the long-term group, but only 50 and 45%, respectively, in the short-term group. Nine patients (45%) relapsed in the short-term group after tacrolimus withdrawal, while not a single patient suffered recurrence in the long-term group. The concentration of tacrolimus remained similar between the two groups at 5-8 ng/ml during the initial 6 months, and was significantly decreased at 12 months compared to 6 months (p < 0.05), along with reduction of oral administration in the long-term group. CONCLUSION: Combined therapy of tacrolimus with prednisone can relieve IMN significantly; prolonged tacrolimus treatment at a low blood concentration can alleviate the illness persistently, with a low recurrence rate and gratifying safety.

Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy.

TGF-ß1 upregulates microRNA-192 (miR-192) in cultured glomerular mesangial cells and in glomeruli from diabetic mice. miR-192 not only increases collagen expression by targeting the E-box repressors Zeb1/2 but also modulates other renal miRNAs, suggesting that it may be a therapeutic target for diabetic nephropathy. We evaluated the efficacy of a locked nucleic acid (LNA)-modified inhibitor of miR-192, designated LNA-anti-miR-192, in mouse models of diabetic nephropathy. LNA-anti-miR-192 significantly reduced levels of miR-192, but not miR-194, in kidneys of both normal and streptozotocin-induced diabetic mice. In the kidneys of diabetic mice, inhibition of miR-192 significantly increased Zeb1/2 and decreased gene expression of collagen, TGF-ß, and fibronectin; immunostaining confirmed the downregulation of these mediators of renal fibrosis. Furthermore, LNA-anti-miR-192 attenuated proteinuria in these diabetic mice. In summary, the specific reduction of renal miR-192 decreases renal fibrosis and improves proteinuria, lending support for the possibility of an anti-miRNA-based translational approach to the treatment of diabetic nephropathy.

Research progress of nephrotic syndrome accompanied by thromboembolism.

Thromboembolism (TE) is a common and serious complication of nephrotic syndrome (NS). NS is associated with hypercoagulability, which may be induced by changes in coagulation, anticoagulant, and fibrinolytic factors. Moreover, accumulating evidence supports the hypothesis that the complex interactions between genetic and acquired risk factors in TE should be considered and that genetic susceptibility should not be ignored. Extracellular vesicles (EVs) also play unique roles. Further research on EVs may provide new insights into the discovery and treatment of TE associated with NS. The occurrence of NS accompanied by TE may be associated with various risk factors. Preventive anticoagulant therapy can not only reduce the risk of TE in patients but also aggravate the risk of bleeding. Heparin and vitamin K antagonists (VKAs), traditional anticoagulant drugs, have been extensively applied in the prevention and treatment of thromboembolic diseases, and emerging direct oral anticoagulants (DOACs) also provide an alternative choice. Owing to the particularity of NS, the safe application of DOACs still needs to be addressed. This review aimed to comprehensively describe the pathophysiology of TE in NS, as well as analyze the associated risk factors, the opportunity for preventive anticoagulation, and current anticoagulant information.

Flavin mononucleotide in visible light photoinitiating systems for multiple-photocrosslinking and photoencapsulation strategies.

Visible light-induced photocrosslinking techniques have attracted significant attention for their flexibility, controllability, safety, and energy conservation, especially in tissue engineering and biofabrication, compared to UV photocrosslinking. Despite these advantages, current photoinitiators are constrained by various challenges, including inadequate photoinitiation efficiency, low biocompatibility, poor water solubility, and limited compatibility with diverse crosslinking systems. Here, a water-soluble derivative of riboflavin, flavin mononucleotide (FMN-), was used to assess its potential as an initiator in multiple-photocrosslinking systems, including radical photopolymerization, dityrosine, and ditryptophan coupling crosslinking, under blue light irradiation. Blue light irradiation facilitated an efficient electron transfer reaction between FMN- and persulfate, owing to their suitable spectral compatibility and photoactivity. The resulting oxidizing free radicals and excited triplet state of FMN- served as initiating active species for the multiple-photocrosslinking reactions. The combination of FMN- and potassium persulfate (KPS) exhibited exceptional photoinitiation efficiency for various biomaterials, including silk fibroin, gelatin, poly(ethylene glycol) diacrylate, and carboxymethyl cellulose modified with amino acids. Furthermore, the cytocompatibility of the FMN-/KPS photoinitiator was demonstrated by the survival rates of 3T3-LI fibroblasts encapsulated in it, which exceeded 95 % when compared to a commercial initiator. STATEMENT OF SIGNIFICANCE: By introducing persulfate, the photoinitiation efficiency of flavin mononucleotide was significantly improved. The application scenarios of flavin mononucleotide and persulfate combinations were also greatly extended, including radical photopolymerization, dityrosine, diphenylalanine, and ditryptophan coupling crosslinking. Among them, the coupling crosslinking of amino acids (di-phenylalanine, and di-tryptophan) modified carboxymethyl cellulose, to our knowledge, was first reported. The excellent cytocompatibility of cell encapsulation further proved that the combinations of flavin mononucleotide and persulfate have great potential in tissue engineering.

Facile Preparation of Dense Polysulfone UF Membranes with Enhanced Salt Rejection by Post-Heating.

Polysulfone (PSf) membranes typically have a negligible rejection of salts due to the intrinsic larger pore size and wide pore size distribution. In this work, a facile and scalable heat treatment was proposed to increase the salt rejection. The influence of heat treatment on the structure and performance of PSf membranes was systematically investigated. The average pore size decreased from 9.94 ± 5.5 nm for pristine membranes to 1.18 ± 0.19 nm with the increase in temperature to 50 °C, while the corresponding porosity decreased from 2.07% to 0.13%. Meanwhile, the thickness of the sponge structure decreased from 20.20 to 11.5 µm as the heat treatment temperature increased to 50 °C. The MWCO of PSf decreased from 290,000 Da to 120 Da, whereas the membrane pore size decreased from 5.5 to 0.19 nm. Correspondingly, the water flux decreased from 1545 to 27.24 L·m-2·h-1, while the rejection ratio increased from 3.1% to 74.0% for Na2SO4, from 1.3% to 48.2% for MgSO4, and from 0.6% to 23.8% for NaCl. Meanwhile, mechanism analysis indicated that the water evaporation in the membranes resulted in the shrinkage of the membrane pores and decrease in the average pore size, thus improving the separation performance. In addition, the desalting performance of the heat-treated membranes for real actual industrial wastewater was improved. This provides a facile and scalable route for PSf membrane applications for enhanced desalination.

Relationship between five GLUT1 gene single nucleotide polymorphisms and diabetic nephropathy: a systematic review and meta-analysis.

So far, case-control studies on the association between glucose transporter 1 (GLUT1) gene single nucleotide polymorphisms (SNPs) and diabetic nephropathy (DN) have generated considerable controversy. To clarify the linkage of GLUT1 SNPs on the risk of DN, a systematic review and meta-analysis was performed. A comprehensive literature search of electronic databases was conducted to obtain relative studies. Nine case-control studies were included. Significant differences were found between XbaI SNP (rs841853) and increased risk of DN in all genetic models. Subgroup analyses for Caucasians population and DN from both type 1 and type 2 diabetes also revealed positive results. For Enh2-1 SNP (rs841847), Enh2-2 SNP (rs841848) and HaeIII SNP (rs1385129), obvious linkages were demonstrated in recessive model. However, analysis for the association between HpyCH4V SNP (rs710218) and the susceptibility of DN showed no significance. Likewise, negative outcome was also found in the assessment for the influence of XbaI or Enh2-2 SNP on the pathogenesis progress of DN. The evidence currently available shows that XbaI, Enh2 and HaeIII SNPs, but not HpyCH4V SNP, in GLUT1 gene may be genetic susceptibility to DN. However, data does not support the association between either XbaI or Enh2-2 SNP and the severity of DN.

Negative correlations between cultivable and active-yet-uncultivable pyrene degraders explain the postponed bioaugmentation.

Bioaugmentation is an effective approach to remediate soils contaminated by polycyclic aromatic hydrocarbons (PAHs), but suffers from unsatisfactory performance in engineering practices, which is hypothetically explained by the complicated interactions between indigenous microbes and introduced degraders. This study isolated a cultivable pyrene degrader (Sphingomonas sp. YT1005) and an active pyrene degrading consortium (Gp16, Streptomyces, Pseudonocardia, Panacagrimonas, Methylotenera and Nitrospira) by magnetic-nanoparticle mediated isolation (MMI) from soils. Pyrene biodegradation was postponed in bioaugmentation with Sphingomonas sp. YT1005, whilst increased by 30.17% by the active pyrene degrading consortium. Pyrene dioxygenase encoding genes (nidA, nidA3 and PAH-RHDα-GP) were enriched in MMI isolates and positively correlated with pyrene degradation efficiency. Pyrene degradation by Sphingomonas sp. YT1005 only followed the phthalate pathway, whereas both phthalate and salicylate pathways were observed in the active pyrene degrading consortium. The results indicated that the uncultivable pyrene degraders were suitable for bioaugmentation, rather than cultivable Sphingomonas sp. YT1005. The negative correlations between Sphingomonas sp. YT1005 and the active-yet-uncultivable pyrene degraders were the underlying mechanisms of bioaugmentation postpone in engineering practices.

Post-transcriptional up-regulation of Tsc-22 by Ybx1, a target of miR-216a, mediates TGF-{beta}-induced collagen expression in kidney cells.

Increased accumulation of extracellular matrix proteins and hypertrophy induced by transforming growth factor-ß1 (TGF-ß) in renal mesangial cells (MC) are hallmark features of diabetic nephropathy. Although the post-transcriptional regulation of key genes has been implicated in these events, details are not fully understood. Here we show that TGF-ß increased microRNA-216a (miR-216a) levels in mouse MC, with parallel down-regulation of Ybx1, a miR-216a target and RNA-binding protein. TGF-ß also enhanced protein levels of Tsc-22 (TGF-ß-stimulated clone 22) and collagen type I α-2 (Col1a2) expression in MC through far upstream enhancer E-boxes by interaction of Tsc-22 with an E-box regulator, Tfe3. Ybx1 colocalized with processing bodies in MC and formed a ribonucleoprotein complex with Tsc-22 mRNA, and this complex formation was reduced by TGF-ß, miR-216a mimics, or Ybx1 shRNA to increase Tsc-22 protein levels but enhanced by miR-216a inhibitor oligonucleotides. Chromatin immunoprecipitation (ChIP) assays revealed that TGF-ß could increase the occupancies of Tsc-22 and Tfe3 on enhancer E-boxes of Col1a2. Co-immunoprecipitation assays revealed that TGF-ß promoted the interaction of Tsc-22 with Tfe3. These results demonstrate that post-transcriptional regulation of Tsc-22 mediated through Ybx1, a miR-216a target, plays a key role in TGF-ß-induced Col1a2 in MC related to the pathogenesis of diabetic nephropathy.

Epigenetic histone methylation modulates fibrotic gene expression.

TGF-ß1-induced expression of extracellular matrix (ECM) genes plays a major role in the development of chronic renal diseases such as diabetic nephropathy. Although many key transcription factors are known, mechanisms involving the nuclear chromatin that modulate ECM gene expression remain unclear. Here, we examined the role of epigenetic chromatin marks such as histone H3 lysine methylation (H3Kme) in TGF-ß1-induced gene expression in rat mesangial cells under normal and high-glucose (HG) conditions. TGF-ß1 increased the expression of the ECM-associated genes connective tissue growth factor, collagen-α1[Ι], and plasminogen activator inhibitor-1. Increased levels of chromatin marks associated with active genes (H3K4me1, H3K4me2, and H3K4me3), and decreased levels of repressive marks (H3K9me2 and H3K9me3) at these gene promoters accompanied these changes in expression. TGF-ß1 also increased expression of the H3K4 methyltransferase SET7/9 and recruitment to these promoters. SET7/9 gene silencing with siRNAs significantly attenuated TGF-ß1-induced ECM gene expression. Furthermore, a TGF-ß1 antibody not only blocked HG-induced ECM gene expression but also reversed HG-induced changes in promoter H3Kme levels and SET7/9 occupancy. Taken together, these results show the functional role of epigenetic chromatin histone H3Kme in TGF-ß1-mediated ECM gene expression in mesangial cells under normal and HG conditions. Pharmacologic and other therapies that reverse these modifications could have potential renoprotective effects for diabetic nephropathy.

Denitrification characteristics of a marine origin psychrophilic aerobic denitrifying bacterium.

A psychrophilic aerobic denitrifying bacterium, strain S1-1, was isolated from a biological aerated filter conducted for treatment of recirculating water in a marine aquaculture system. Strain S1-1 was preliminarily identified as Psychrobacter sp. based on the analysis of its 16S rRNA gene sequence, which showed 100% sequence similarity to that of Psychrobacter sp. TSBY-70. Strain S1-1 grew well either in high nitrate or high nitrite conditions with a removal of 100% nitrate or 63.50% nitrite, and the total nitrogen removal rates could reach to 46.48% and 31.89%, respectively. The results indicated that nitrate was mainly reduced in its logarithmic growth phase with a very low level accumulation of nitrite, suggesting that the aerobic denitrification process of strain S1-1 occurred mainly in this phase. The GC-MS results showed that N2O was formed as the major intermediate during the aerobic denitrifying process of strain S1-1. Finally, factors affecting the growth of strain S1-1 and its aerobic denitrifying ability were also investigated. Results showed that the optimum aerobic denitrification conditions for strain S1-1 were sodium succinate as carbon source, C/N ratio15, salinity 10 g/L NaCl, incubation temperature 20 degrees C and initial pH 6.5.

The role of extracellular vesicles in podocyte autophagy in kidney disease.

Podocytes are the key cells involved in protein filtration in the glomerulus. Once proteins appear in the urine when podocytes fail, patients will end with renal failure due to the progression of glomerular damage if no proper treatment is applied. The injury and loss of podocytes can be attributed to diverse factors, such as genetic, immunologic, toxic, or metabolic disorders. Recently, autophagy has emerged as a key mechanism to eliminate the unwanted cytoplasmic materials and to prolong the lifespan of podocytes by alleviating cell damage and stress. Typically, the fundamental function of extracellular vesicles (EVs) is to mediate the intercellular communication. Recent studies have suggested that, EVs, especially exosomes, play a certain role in information transfer by communicating proteins, mRNAs, and microRNAs with recipient cells. Under physiological and pathological conditions, EVs assist in the bioinformation interchange between kidneys and other organs. It is suggested that EVs are related to the pathogenesis of acute kidney injury and chronic kidney disease, including glomerular disease, diabetic nephropathy, renal fibrosis and end-stage renal disease. However, the role of EVs in podocyte autophagy remains unclear so far. Here, this study integrated the existing information about the relevancy, diagnostic value and therapeutic potential of EVs in a variety of podocytes-related diseases. The accumulating evidence highlighted that autophagy played a critical role in the homeostasis of podocytes in glomerular disease.

Cross-Linked Covalent Organic Framework-Based Membranes with Trimesoyl Chloride for Enhanced Desalination.

The rational design of continuous covalent organic framework (COF)-based membranes is challenging for desalination applications, mainly due to the larger intrinsic pore size of COFs and defects in the crystalline film, which lead to a negligible NaCl rejection ratio. In this work, we first demonstrated a COF-based desalination membrane with in situ cross-linking of a COF-TpPa layer by trimesoyl chloride (TMC) to stitch the defects between COF crystals and cross-link the COF cavity with high-cross-linking degree networks to enhance NaCl rejection. With the addition of TMC monomers, both small spherical nodules and some elongated "leaf-like" features were observed on the membrane surface due to the appearance of nanovoids during cross-linking. The resulting COF-based desalination membrane had a water permeability of approximately 0.81 L m-2 h-1 bar-1 and offered substantial enhancement of the NaCl rejection ratio from being negligible to 93.3% at 5 bar. Mechanistic analysis indicated that the amidation reaction of the secondary amine in keto COF with TMC induced the formation of a highly porous network structure both in the cavity and on the exterior of COF, thereby successfully forming a continuous and nanovoid-containing selective layer for desalination. In addition, the membrane exhibited excellent desalting performance for real industrial wastewater with both low and high salinity. This study proposed that the introduction of a cross-linker to react with the terminal amine group and secondary amine in the backbone of the keto form of COF or its derivatives could provide a facile and scalable approach to fabricate a COF-based membrane with superior NaCl rejection. This opens a new fabrication route for COF-based desalination membranes, as well as extended applications in water desalination.

Detection of microRNA-33a-5p in serum, urine and renal tissue of patients with IgA nephropathy.

The present study aimed to detect the levels of microRNA (miR)-33a-5p in the renal tissue, serum and urine of patients with primary IgA nephropathy (IgAN), thereby preliminarily exploring the association between the levels of miR-33a-5p and the condition of primary IgAN to provide evidence for the expression of miR-33a-5p in the serum and urine of IgAN patients as a clinical marker. Reverse-transcription quantitative PCR was performed to evaluate the level of miR-33a-5p in IgAN patients according to severity and pathological classification. The results suggested that the levels of miR-33a-5p in the serum, urine and kidney tissues of patients with IgAN were lower than those of the control tissues obtained from cancer patients (0.28±0.25 vs. 1.00±0.45, P<0.05; 0.34±0.28 vs. 1.00±0.53, P<0.05; 0.47±0.27 vs. 1.00±0.38, P<0.05, respectively). Receiver operating characteristic curve analysis suggested that the serum and urine levels of miR-33a-5p may be used as a marker to differentiate renal injury in IgAN patients from healthy individuals. At the same time, according to the estimated glomerular filtration rate (eGFR) and Lee classification of nephropathy, it was determined that with the progression of renal failure and the increase of the pathological grade of kidney tissue, the relative level of miR-33a-5p in kidney tissue also decreased (eGFR <50 ml/min vs. eGFR ≥50 ml/min/1.73 m2 group: 0.38±0.27 vs. 1.00±0.34, P<0.001; Lee grade ≤3 group vs. Lee grade >3: 1.00±0.48 vs. 0.38±0.45, P<0.05). This result suggested that the levels of miR-33a-5p in serum, urine and kidney tissues decreased with the severity of renal injury and the progression of renal failure in patients with IgAN. Hence, miR-33a-5p detected in the serum and urine may be used as a non-invasive biomarker to reflect the progression of renal injury and renal failure in patients with IgAN.