Superefficient Removal of Heavy Metals from Wastewater by Mg-Loaded Biochars: Adsorption Characteristics and Removal Mechanisms.

Six types of biochar (BSB, CSB, FSB, CFSB, MSB, and TSB) were prepared from different raw materials by loading magnesium ions (Mg2+) via an impregnation process. The adsorption kinetics and thermodynamics of heavy metals at high concentrations were analyzed. The adsorption mechanisms were investigated by zeta potential, scanning electron microscopy-energy-dispersive X-ray spectroscopy, Fourier-transform infrared spectroscopy, X-ray diffraction, X-ray photoelectron spectroscopy, and inductively coupled plasma-atomic absorption spectroscopy analyses. The adsorption of heavy metals by BSB, CSB, FSB, CFSB, MSB, and TSB conformed to the Langmuir model and PS-order. The maximum theoretical saturation adsorption capacities for Cd(II), Cu(II), and Pb(II) were 333.33, 238.10, 75.19, 96.15, 66.23, and 185.19 mg·g-1; 370.37, 294.12, 111.11, 169.49, 84.75, and 217.39 mg·g-1; and 302.58, 200.00, 61.73, 90.91, 54.47, and 166.67 mg·g-1, respectively. According to the analysis of the contribution of adsorption, the adsorption process was mainly controlled by cation-π interactions, ion exchange, mineral precipitation, and functional group interactions. Biochars contain ash, functional groups and load a large number of Mg2+, which can form complexes with metal ions and perform strong ion exchange; therefore, mineral precipitation and cation exchange played dominant roles in the adsorption process. The prepared Mg-loaded biochars presented in this research showed excellent adsorption properties for heavy metals and have great potential for practical application; in particular, BSB had the strongest adsorption capacity for the three heavy metal ions.

Rare, low-frequency and common coding variants of ARHGEF28 gene and their association with sporadic amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Over 90% of cases are sporadic (sALS) and 5%-10% are familial (fALS). So far, more than 20 genes/loci have been linked to ALS. C9orf72, SOD1, TARDBP, and FUS are noted as the most common ALS genes; however, mutations of these genes explain <10% of sALS cases. Recently, Rho guanine nucleotide exchange factor, encoded by ARHGEF28, has been linked to the ALS pathogenesis, possibly by binding low-molecular-weight neurofilament mRNA and affects its stability. However, a systemic screening of ARHGEF28 mutations in ALS is lacking. In this study, we sequenced the entire coding sequence of ARHGEF28 in a Chinese cohort of 399 sporadic ALS and 327 elderly controls. A total of 73 coding variants were identified, including 26 synonymous and 47 nonsynonymous. Among the nonsynonymous variants, 33 were rare (minor allele frequency [MAF]<0.01), in which 18 were only identified in cases and 12 were only in controls. Three loss-of-function mutations were identified, including 2 truncations (p.Arg231Ter and p.Ser561Ter) and a frameshift deletion (p.Lys1070fs) in 2 cases and 1 control subject. The frequency of total and case-only rare variants was 7.5% (30/399) and 5.0% (20/399), respectively, in the patients. SKAT-O test suggested that the novel coding variants were marginally enriched in the cases (p = 0.049). Single-variant analysis suggested that the p.Asn1046Ser variant had a higher frequency in cases (8/399, 0.02) than in controls (1/327, 0.003) (OR: 6.67, 95% CI: 0.83-53.61; p = 0.046). By contrast, none of the low-frequency (MAF: 0.01-0.05) or common (MAF > 0.05) variants was associated with ALS (p > 0.05). Among all patients, 9 (2.3%) carried rare variants predicted to be deleterious, and the age at onset of these carriers (45.6 ± 10.9 years) was marginally younger than noncarriers (51.9 ± 10.7 years) (p = 0.11). Our results supported a possible genetic contribution of rare but not low-frequency and common coding variants to ALS. These data may have implications in the mechanisms and genetic counseling of the disease.

Phosphate adsorption from wastewater using ZnAl-LDO-loaded modified banana straw biochar.

ZnAl-layered double hydroxide-loaded banana straw biochar (ZnAl-LDH-BSB) was prepared via the hydrothermal method, and the efficient phosphorus removal agent ZnAl-LDO-BSB was obtained by calcination at 500 °C. Based on the ZnAl-LDO-BSB adsorption characteristics, the adsorption mechanism was evaluated via TG/DTA, FTIR, XRD, SEM, HRTEM, and other characterization methods. The results showed that the ZnAl-LDO-BSB assembled into microspheres with typical hexagonal lamellar structures and presented good thermal stability. The adsorption of total phosphate (TP) by ZnAl-LDO-BSB conforms to the Langmuir model, and the theoretical maximum adsorption capacity is 185.19 mg g-1. The adsorption kinetics were in accordance with the second-order kinetic model, and the anion influence on TP adsorption followed the order CO32- > SO42- > NO3-. The combination of zeta potential measurements with the FTIR, XRD, SEM, HRTEM, and XPS results suggested that ZnAl-LDO-BSB adsorbs TP mainly by electrostatic adsorption, surface coordination, and anion intercalation. Graphical abstract.

Characteristics of nitrogen and phosphorus adsorption by Mg-loaded biochar from different feedstocks.

Herein, biochars from 6 different feedstocks (taro straw, corn straw, cassava straw, Chinese fir straw, banana straw, and Camellia oleifera shell) were produced using magnesium chloride (MgCl2) as a modifier due to their sorption behavior toward NH4+-N and phosphorus in an aqueous solution. The biochar characteristics were evaluated, including pH, pHPZC, biochar magnesium content, and total pore volume (PVtot). The experimental results in terms of the kinetics and equilibrium isotherms showed that the cassava straw and banana straw biochars exhibited the theoretical maximum saturated adsorption capacities of 24.04 mg·g-1 (NH4+-N) and 31.15 mg·g-1 (TP), respectively. Biochar produced from these feedstocks had higher magnesium contents and greater total pore volumes, reflecting the significant contributions from magnesium and steric effects. FTIR, XRD, and SEM/EDS analyses demonstrated that NH4+-N and TP sorption mechanisms predominantly involved surface electrostatic attraction, Mg2+ precipitates and complexation with surface hydroxyl functional groups.

Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells.

BACKGROUND: Parkinson's disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old. Mitochondrial defects and oxidative stress actively participate in degeneration of dopaminergic (DA) neurons in PD. Paeonolum, a main component isolated from Moutan cortex, has potent antioxidant ability. Here, we have examined the effects of paeonolum against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells. METHODS: The overall viability and neurodegeneration of DA neurons was assessed in ETvmat2:green fluorescent protein (GFP) transgenic zebrafish, in which most monoaminergic neurons are labeled by GFP. Damage to PC12 cells was measured using a cell viability assay and assessment of nuclear morphology. Intracellular reactive oxygen species (ROS) and the level of total GSH were assessed. The mitochondrial cell death pathway including mitochondrial membrane potential, cytochrome C release and caspase-3 activity were also examined in PC12 cells. RESULTS: Paeonolum protected against MPP(+)-induced DA neurodegeneration and locomotor dysfunction in zebrafish in a concentration-dependent manner. Similar neuroprotection was replicated in the PC12 cellular model of MPP(+) toxicity. Paeonolum attenuated MPP(+)-induced intracellular ROS accumulation and restored the level of total GSH in PC12 cells. Furthermore, paeonolum significantly inhibited the mitochondrial cell death pathway induced by MPP(+). CONCLUSIONS: Collectively, the present study demonstrates that paeonolum protects zebrafish and PC12 cells against MPP(+)-induced neurotoxicity.

Absence of mutations in exon 6 of the TARDBP gene in 207 Chinese patients with sporadic amyotrohic lateral sclerosis.

Mutations in the TARDBP gene, which encodes the Tar DNA binding protein, have been shown to causes of both familial amyotrophic lateral sclerosis (FALS) and sporadic ALS (SALS). Recently, several novel TARDBP exon 6 mutants have been reported in patients with ALS in Europe and America but not in Asia. To further examine the spectrum and frequency of TARDBP exon 6 mutations, we investigated their frequency in ethnic Chinese patients with sporadic ALS. TARDBP exon 6 was screened by direct sequencing in 207 non-SOD1 SALS patients and 230 unrelated healthy controls but no mutations were identified. Our data indicate that exon 6 mutations in TARDBP are not a common cause of SALS in Han Chinese population from Southern Mainland China.

Motoneuron differentiation of induced pluripotent stem cells from SOD1G93A mice.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder mainly affecting motor neurons. Mutations in superoxide dismutase-1 (SOD-1) account for about 20% of familial ALS patients. A robust supply of motoneurons carrying the mutated gene would help understand the causes of motoneuron death and develop new therapeutics for the disease. Here, we established induced pluripotent stem (iPS) cell lines from SOD1G93A mice and compared their potency in motoneuron generation with normal iPS cells and mouse embryonic stem cells (E14). Our results showed that iPS cells derived from SOD1G93A mice possessed the similar potency in neuronal differentiation to normal iPS cells and E14 cells and can be efficiently driven to motoneuron-like phenotype. These cells exhibited typical neuronal morphology, expressed key motoneuron markers, including ChAT and HB9, and generated repetitive trains of action potentials. Furthermore, these neurons highly expressed human SOD-1 and exhibited shorter neurites compared to controls. The present study provides evidence that ALS-iPS cells can be used as disease models in high-throughput screening and mechanistic studies due to their ability to efficiently differentiate into specific neuronal subtypes.

Marine cyclotripeptide X-13 promotes angiogenesis in zebrafish and human endothelial cells via PI3K/Akt/eNOS signaling pathways.

Cyclotripeptide X-13 is a core of novel marine compound xyloallenoide A isolated from mangrove fungus Xylaria sp. (no. 2508). We found that X-13 dose-dependently induced angiogenesis in zebrafish embryos and in human endothelial cells, which was accompanied by increased phosphorylation of eNOS and Akt and NO release. Inhibition of PI3K/Akt/eNOS by LY294002 or L-NAME suppressed X-13-induced angiogenesis. The present work demonstrates that X-13 promotes angiogenesis via PI3K/Akt/eNOS pathways.

Neuronal differentiation potential of mouse induced pluripotent stem cells.

Induced pluripotent stem (iPS) cells have been generated from somatic cells by ectopic expression of defined transcription factors. The important issues for clinical applications of iPS cells are the defined methods for somatic cell differentiation and how to effectively enrich desired cell population. Here we used humanized renilla green fluorescent protein under the control of Tα1 α-tubulin promoter as lineage selection marker for neuronal differentiation of iPS cells. Using fluorescence-activated cell sorting, green fluorescent protein positive cells were isolated and enriched to near-purity. These results indicated that the neuronal differentiation potential of iPS cells derived from adult somatic cells is similar to that of embryonic stem cells and the high-purity neurons may have important implications for neurodevelopmental studies, safety pharmacological studies, and transplantation studies.

[Protective effects of Lycium barbarum extract against MPP(+) -induced neurotoxicity in Caenorhabditis elegans and PC12 cells].

OBJECTIVE: To investigate the neuroprotective effects of Lycium barbarum extract against MPP(+) -induced neurotoxicity in Caenorhabditis elegans and PC12 cells and its mechanism. METHODS: Pretreated MPP(+) -induced nearotoxicity in C. elegans and PC12 cells with Lycium barbarum at different dosages. The viability and DA neurodegeneration was assessed in C. elegans selectively expressing green fluorescent protein (GFP) in DA neurons. PC12 cell damage was measured using MTT and nuclear morphology. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential and total GSH were assessed. RESULTS: Lycium barbarum extract protected against MPP(+) -induced loss of viability and DA neurodegeneration in C. elegans in a dose-dependent manner. Similar neuroprotection was replicated in MPP + PC12 cell model. Lycium barbarum extract attenuated MPP(+) -induced intracellular ROS accumulation, loss of mitochondrial membrane potential and restored total GSH levels in PCl2 cells. CONCLUSIONS: Lycium barbarum extract protects against MPP(+) -induced neurotoxicity in C. elegans and PC12 cells and its machanism may be related to its antioxidative property and restoration of total GSH level.