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Enhancing antimicrobial activity is an effective strategy to mitigate membrane biofouling. In this study, an antimicrobial electrospun polyacrylonitrile (PAN) nanofiber mat decorated with in situ synthesized silver nanoparticles (AgNPs) was developed as support for a thin-film composite forward osmosis (FO) membrane. Effects of AgNPs on the physicochemical properties, water flux, reverse salt flux, and antimicrobial activity of the FO membrane were investigated, and also the antimicrobial mechanism was explored. Results showed AgNPs were monodisperse in the nanofibers, and the Ag/PAN nanofiber support (Ag/PAN-NFS) had a scaffoldlike structure which could reduce internal concentration polarization. The Ag/PAN-NFS supported thin-film nanocomposite (Ag/PAN-TFN) FO membrane demonstrated outstanding hydrophilicity, resulting in high water fluxes in both FO and PRO modes. The Ag/PAN-TFN FO membranes, even the one with the lowest silver content of 0.5 wt %, exhibited excellent antibacterial activities for E. coli (96%) and S. aureus (92%), which was mainly due to the Ag + -species released into the solution.

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The early prediction of renal outcomes in patients with idiopathic membranous nephropathy (iMN) remains challenging. The present retrospective study evaluated patients with iMN confirmed by renal biopsy. An optimized Cox regression model and a nomogram were constructed for the early prediction of renal outcomes. A total of 141 patients who met the inclusion criteria were evaluated in the present study. In total 18 (12.8%) patients eventually progressed to the endpoint, 6 of whom developed end-stage renal disease, and one patient died during follow-up. The optimized model demonstrated that 24-h proteinuria [hazard ratio (HR) 1.24; 95% CI, 1.10-1.40; P-value <0.001] and chronic tubulointerstitial injury [referred to as grade 0, grade 1 (HR), 5.12; 95% CI, 1.33-19.75; P-value= 0.02] or grade 2 (HR, 6.43; 95% CI, 1.35-30.59; P-value= 0.02) were independent risk factors for a poor renal outcome. Patients with an estimated three-year renal survival rate (ETR) less than 0.87 had a high risk of a poor renal outcome. In addition, patients with an ETR of 0.87 to 0.98 more quickly developed a decreased estimated glomerular filtration rate after two years of follow-up. In the present study a nomogram for the early prediction of renal outcomes in patients with iMN was developed. This nonogram suggested that patients with an ETR of 0.87-0.98 should receive greater attention during follow-up.

A novel root-specific gene and its upstream promoter were cloned and characterized for potential application in root-specific expression of transgenes. The root is an important plant organ subjected to many biotic and abiotic stresses, such as infection by Ralstonia solanacearum. To isolate tobacco root-specific promoters for genetic applications, microarray screening was performed to identify genes highly and specifically expressed in the root. One root-specific gene encoding an extensin-like protein (NtREL1) was isolated, and its expression pattern was further characterized by both microarray analysis and reverse transcription-polymerase chain reaction. NtREL1 was highly expressed only in roots but not in any other organ. NtREL1 expression was affected by hormone treatment (salicylic acid, abscisic acid, and ethephon) as well as low temperature, drought, and R. solanacearum infection. A full-length 849 bp cDNA containing a 657-nucleotide open reading frame was cloned by Rapid Amplification of cDNA Ends. Subsequently, a fragment of 1,574 bp upstream of NtREL1 was isolated by flanking PCR and named pNtREL1. This promoter fragment contains TATA, GATA, and CAAT-boxes, the basic elements of a promoter, and six root-specific expression elements, namely OSE1, OSE2, ROOTMOTIFTAPOX1, SURECOREATSULTR11, P1BS, and WUSATAg. A construct containing the bacterial uidA reporter gene (β-glucuronidase, GUS) driven by the pNtREL1 promoter was transformed into tobacco plants. GUS staining was only detected in the root, but not in leaves and stems. Additionally, transgenic tobacco plants containing peanut resveratrol synthase gene (AhRS) driven by the pNtREL1 promoter produced resveratrol only in the root. Thus, the pNtREL1 promoter can be used to direct root-specific expression of target genes to protect the root from stress or for biological studies.

Background: WNK kinase is a serine/threonine kinase that plays an important role in normal blood pressure homeostasis. WNK3 was previously found to enhance the activity of sodium chloride cotransporter (NCC) in Xenopus oocyte. However, the mechanism through which it works remains unclear. Methods: Using overexpression and siRNA knock-down techniques, the effects of WNK3 on NCC in both Cos-7 and mouse distal convoluted cells were analyzed by Western blot. Results: We found that WNK3 significantly increased NCC protein expression in a dose-dependent manner. NCC protein expression in Cos-7 cells was markedly decreased after 2 h treatment with protease inhibitor, cycloheximide (CHX) in the NCC alone group, but was significantly decreased after 8 h treatment of CHX in the WNK3 + NCC group. WNK3 significantly increased NCC protein expression in both NCC alone and WNK3 + NCC groups regardless the overnight treatments of bafilomycin A1, a proton pump inhibitor, suggesting that WNK3-mediated increased NCC expression is not dependent on the lysosomal pathway. We further found that WNK3 group had a quicker NCC recovery than the control group using CHX pulse assay, suggesting that WNK3 increases NCC protein synthesis. WNK3 enhanced NCC protein level while reducing ERK 1/2 phosphorylation. In addition, knock-down of ERK 1/2 expression reversed WNK3-mediated increase of NCC expression. Conclusion: These results suggest that WNK3 enhances NCC protein expression by increasing NCC synthesis via an ERK 1/2-dependent signaling pathway.

Obesity is positively linked to multiple metabolic complications including renal diseases. Several studies have demonstrated Kruppel‐like factor 4 (KLF4) participated in renal dysfunction and structural disorders in acute kidney injuries, but whether it affected the process of chronic kidney diseases was unknown. Therefore, present study was to disclose the role of renal KLF4 in dietary‐induced renal injuries and underlying mechanisms in obesity. Through utilizing high‐fat diet‐fed mice and human renal biopsies, we provided the physiological roles of KLF4 in protecting against obesity‐related nephropathy. Decreased levels of renal KLF4 were positively correlated with dietary‐induced renal dysfunction, including increased levels of creatinine and blood urea nitrogen. Overexpression of renal KLF4 suppressed inflammatory response in palmitic acid‐treated mouse endothelial cells. Furthermore, overexpressed KLF4 also attenuated dietary‐induced renal functional disorders, abnormal structural remodelling and inflammation. Mechanistically, KLF4 maintained renal mitochondrial biogenesis and activities to combat obesity‐induced mitochondrial dysfunction. In clinical renal biopsies and plasma, the renal Klf4 level was negatively associated with circulating levels of creatinine but positively associated with renal creatinine clearance. In conclusions, the present findings firstly supported that renal KLF4 played an important role in combating obesity‐related nephropathy, and KLF4/mitochondrial function partially determined the energy homeostasis in chronic kidney diseases.

Dear Editor, NCC (Na-Cl cotransporter) is a cotransporter mainly distributed in the distal tubule of the kidney, functioning to reabsorb sodium and chloride ions from the tubular fluid into the cells of the renal distal convoluted tubule. It is a transmembrane protein belonging to the SLC12 cotransporter family of electro-neutral cation-coupled chloride cotransporters, which is closely related to hypertension (Gamba, 2005). A loss of NCC function can cause Gitelman syndrome, a disease characterized by low blood pressure, hypocalciuria, hypokalemic metabolic alkalosis, and hypomagnesemia, etc. WNK3 (With No Lysine K 3) is highly expressed in the whole length of the renal tubules (Glover et al., 2009). It was previously found to enhance the activity of NCC in Xenopus oocyte (Rinehart et al., 2005). Exploring the regulatory effect of WNK3 on NCC may be helpful to understand the occurrence of abnormal renal sodium transporters and provide new targets for the treatment of hypertension. However, whether WNK3 interacts directly with NCC in mammalian cells still remains unclear. In this article, we report the results of our co-immunoprecipitation experiments and confocal observations, confirming that WNK3 does interact with NCC and that the kinase domain of WNK3 plays an important role in the regulation of NCC.To explore whether there is reaction between WNK3 and NCC protein, Cos-7 cells were transfected by GFP-NCC with or without HA-WNK3 and co-immunoprecipitation experiments were performed 48 hours after transfection. As shown in Figure 1, anti-HA antibody with the presence of WNK3 immunoprecipitated NCC whereas serum with the absence of WNK3 did not, suggesting that the WNK3 protein interacts with NCC directly.In order to investigate the effect of WNK3 on NCC, HA-NCC was transfected into Cos-7 cells while increasing doses of HA-WNK3. Western-blot was carried out with anti-HA or anti-GAPDH antibodies 48 h later. The NCC protein expression level gradually increased with the increase of WNK3 dosage ( Figure S1 in Supporting Information). The expression of NCC and WNK3 was checked under a confocal fluorescent microscope ( Figure S2 in Supporting Information). The results showed that WNK3 increased NCC expression both on the cell membrane and in the cytoplasm. It has been confirmed that the enzyme region, the amino terminal, and/or the carboxyl terminal are the key elements of kinase activity. However, whether the enzyme region of WNK3 is necessary in regulating NCC is still unclear. We observed the changes of NCC expression after various WNK3 fragments were transferred into the cells. As shown in Figure S3 in Supporting Information, only the WNK3 fragments containing the enzyme region were able to increase the expression of NCC.WNK kinases belong to a subfamily of serine/threonine kinases. It was reported that the activity of NCC could be down-regulated by WNK4 (Moniz et al., 2010). Our study showed that in the mammalian cells WNK3 was also a chloride sensitive kinase to NCC expression, with its effect being the opposit...