Bio-oxidation of Elemental Mercury into Mercury Sulfide and Humic Acid-Bound Mercury by Sulfate Reduction for Hg0 Removal in Flue Gas.

Bioconversion of elemental mercury (Hg0) into immobile, nontoxic, and less bioavailable species is of vital environmental significance. Here, we investigated bioconversion of Hg0 in a sulfate-reducing membrane biofilm reactor (MBfR). The MBfR achieved effective Hg0 removal by sulfate bioreduction. 16 S rDNA sequencing and metagenomic sequencing revealed that diverse groups of mercury-oxidizing/sulfate-reducing bacteria (Desulfobulbus, Desulfuromonas, Desulfomicrobium, etc.) utilized Hg0 as the initial electron donor and sulfate as the terminal electron acceptor to form the overall redox. These microorganisms coupled Hg0 bio-oxidation to sulfate bioreduction. Analysis on mercury speciation in biofilm by sequential extraction processes (SEPs) and inductively coupled mass spectrometry (ICP-MS) and by mercury temperature programmed desorption (Hg-TPD) showed that mercury sulfide (HgS) and humic acid-bound mercury (HA-Hg) were two major products of Hg0 bio-oxidation. With HgS and HA-Hg comprehensively characterized by X-ray diffraction (XRD), excitation-emission matrix spectra (EEM), scanning electron microscopy-energy disperse spectroscopy (SEM-EDS), X-ray photoelectron spectroscopy (XPS), and Fourier transform infrared spectroscopy (FTIR), it was proposed that biologically oxidized mercury (Hg2+) further reacted with biogenic sulfides to form cubically crystallized metacinnabar (ß-HgS) extracellular particles. Hg2+ was also complexed with functional groups -SH, -OH, -NH-, and -COO- in humic acids from extracellular polymeric substances (EPS) to form HA-Hg. HA-Hg may further react with biogenic sulfides to form HgS. Bioconversion of Hg0 into HgS was therefore achieved and can be a feasible biotechnique for flue gas demercuration.

Research development of the pathogenesis pathways for neuroschistosomiasis.

The infection of the central nervous system (CNS) by schistosome may or may not have clinical manifestations. When symptomatic, neuroschistosomiasis (NS) is one of the most severe presentations of schistosome infection. Among the NS symptoms, cerebral invasion is mostly caused by Schistosoma japonicum (S. japonicum), and the spinal cord symptoms are mainly caused by S. mansoni or S. haematobium. There are 2 main pathways by which schistosomes cause NS: egg embolism and worm migration, via either artery or vein system, especially the valveless perivertebral Batson's plexus. The adult worm migrates anomalously through the above pathways to the CNS where they lay eggs. Due to the differences in species of schistosomes and stages of infection, mechanisms vary greatly. The portal hypertension with hepatosplenic schistosomiasis also plays an important role in the pathogenesis. Here the pathways through which NS occurs in the CNS were reviewed.