Removal of toxic elements from aqueous environments using nano zero-valent iron-and iron oxide-modified biochar:a review

Biochar(BC)has gained attention for removal of toxic elements(TEs)from aqueous media;however,pristine biochar often exhibits low adsorption capability.Thus,various modification strategies in BC have been developed to improve its removal capability against TEs.Nanoscale zero-valent iron(nZVI)and iron oxides(FeOx)have been used as sorbents for TE removal.However,these materials are prone to agglomeration and also expensive,which make their usage limited for large-scale applications.The nZVI technical demerits could be resolved by the development of BC-based composite sorbents through the loading of nZVI or FeOx onto BC surface.Nano zero-valent iron modified BC(nZVIBC),FeOx-modified BC(FeOxBC)have attracted attention for their capability in removing pollutants from the aqueous phases.Nonetheless,a potential use of nZVIBC and FeOxBC for TE removal from aqueous environments has not been well-realized or reviewed.As such,this article reviews:(i)the preparation and characterization of nZVIBC and FeOxBC;(ii)the capacity of nZVIBC and FeOxBC for TE retention in line with their physicochemical properties,and(iii)TE removal mechanisms by nZVIBC and FeOxBC.Adopting nZVI and FeOx in BC increases its sporptive capability of TEs due to surface modifications in morphology,functional groups,and elemental composition.The combined effects of BC and nZVI,FeOx or Fe salts on the sorption of TEs are complex because they are very specific to TEs.This review identified significant opportunities for research and technol-ogy advancement of nZVIBC and FeOxBC as novel and effective sorbents for the remediation of TEs contaminated water.

A Lesion-Mimic Syntaxin Double Mutant in Arabidopsis Reveals Novel Complexity of Pathogen Defense Signaling

The lesion-mimic Arabidopsis mutant, syp121 syp122, constitutively expresses the salicylic acid （SA） signaling pathway and has low penetration resistance to powdery mildew fungi. Genetic analyses of the lesion-mimic phenotype have expanded our understanding of programmed cell death （PCD） in plants. Inactivation of SA signaling genes in syp121 syp122 only partially rescues the lesion-mimic phenotype, indicating that additional defenses contribute to the PCD. Whole genome transcriptome analysis confirmed that SA-induced transcripts, as well as numerous other known pathogenresponse transcripts, are up-regulated after inactivation of the syntaxin genes. A suppressor mutant analysis of syp121 syp122 revealed that FMO1, ALD1, and PAD4 are important for lesion development Mutant alleles of EDS1, NDR1, RAR1, and SGTlb also partially rescued the lesion-mimic phenotype, suggesting that mutating syntaxin genes stimulates TIR-NB-LRR and CC-NB-LRR-type resistances. The syntaxin double knockout potentiated a powdery mildew- induced HR-like response. This required functional PAD4 but not functional SA signaling. However, SA signaling potentiated the PAD4-dependent HR-like response. Analyses of quadruple mutants suggest that EDS5 and SID2 confer separate SA-independent signaling functions, and that FMO1 and ALD1 mediate SA-independent signals that are NPRl-dependent. These studies highlight the contribution of multiple pathways to defense and point to the complexity of their interactions.