Tuning electronic structure of the carbon skeleton to accelerate electron transfer for promoting the capture of gold.

The efficient and selective recovery of gold from secondary sources is key to sustainable development. However, the complexity of the recovery environment can significantly complicate the compositions of utilized sorbents. Here, we report a straw-derived mesoporous carbon as an inexpensive support material. This mesoporous carbon is modified by anions (sulfur modulation, C-S-180) to improve its electron-transfer efficiency and tune the electronic structure of its skeleton toward enhanced gold reduction. The high surface area of C-S-180 (989.4 m2/g), as well as the presence of abundant C-S in the porous structure of the adsorbent, resulted in an outstanding Au3+-uptake capacity (3422.75 mg/g), excellent resistance to interference, and favorable Au3+ selectivity. Dissimilar to most existing carbon-based adsorbents, electrochemistry-based studies on the electron-transfer efficiencies of adsorbents reveal that sulfur modulation is crucial to optimizing their adsorption performances. Furthermore, the density functional theory reveals that the optimization mechanism is attributable to the adjustment of the electronic structure of the carbon skeleton by C-S, which optimizes the band-gap energy for enhanced Au3+ reduction. These findings offer a strategy for constructing green and efficient adsorbents, as well as a basis for extending the applications of inexpensive carbon materials in gold recovery from complex environments.

10­Hydroxycamptothecin induces apoptosis in human fibroblasts by regulating miRNA­23b­3p expression.

10­Hydroxycamptothecin (HCPT) effectively controls epidural fibrosis, but the exact underlying mechanisms remain ambiguous. Abnormal microRNA (miR)­23b­3p expression has been detected in various types of fibrotic tissues that are present in different diseases. The aim of the present study was to elucidate the mechanisms through which HCPT induces fibroblast apoptosis. Reverse transcription­quantitative polymerase chain reactions were performed on six traumatic scar samples and matched normal skin samples; traumatic scar formation was revealed to be significantly inversely associated with miR­23b­3p expression. In addition, the miR­23b­3p expression level in human fibroblasts was examined following HCPT treatment. The effects of HCPT and miR­23b­3p on fibroblast apoptosis were assessed using terminal deoxynucleotidyl­transferase­mediated dUTP nick­end labeling, flow cytometry and western blot analysis. The results demonstrated that HCPT treatment notably increased miR­23b­3p expression levels and accelerated fibroblast apoptosis. Therefore, upregulation of miR­23b­3p expression was demonstrated to promote fibroblast apoptosis, consistently with the effects of HCPT. The results of the present study indicated that HCPT may induce fibroblast apoptosis by regulating miR­23b­3p expression.

CZ2HF mitigates ß-amyloid 25-35 fragment-induced learning and memory impairment through inhibition of neuroinflammation and apoptosis in rats.

Cu­zhi­2­hao­fang (CZ2HF), a traditional Chinese medicine, has been used clinically for the treatment of amnesia. However, whether CZ2HF is capable of alleviating learning and memory impairment in Alzheimer's disease (AD) remains to be elucidated. The present study was designed to explore the effect and mechanism of CZ2HF on ß­amyloid 25­35 (Aß25­35)­induced impairment in the learning and memory of rats. Morris water maze test was used to determine spatial learning and memory ability in Aß25­35­induced AD rats and hippocampal neuronal damage and apoptosis were observed using hematoxylin and eosin staining, Nissl staining and terminal deoxynucleotidyltransferase­mediated dUTP nick­end labeling (TUNEL) assays, respectively. The levels of ß­amyloid 1­42 (Aß1­42), pro­inflammatory factors, such as cyclooxygenase­2 (COX­2), tumor necrosis factor­α (TNF­α) and interleukin­1ß (IL­1ß) and apoptosis­associated genes including B cell leukemia/lymphoma 2 (Bcl­2), Bcl-2­associated X, apoptosis regulator (Bax), pro­caspase­3, inhibitor of κB (IκB­α) degradation and phosphorylated­nuclear factor­κB p65 (p­NF­κB p65) activation were analyzed using western blotting. The findings of the present study revealed that CZ2HF treatment significantly attenuated Aß25­35­induced cognitive impairments in rats. Subsequently, CZ2HF treatment markedly inhibited neuronal damage and deletions. Furthermore, CZ2HF reduced TNF­α, IL­1ß, COX­2 protein expression levels, Bax/Bcl­2 ratio, and reduced Aß1­42 and active­caspase­3 levels. In addition, IκB­α degradation and p­NF­κB p65 activation were reduced by CZ2HF. These findings suggested that CZ2HF treatment improved Aß25­35­induced learning and memory impairment and hippocampal neuronal injury, and its underlying mechanism may be due to the inhibition of neuroinflammation and neuronal apoptosis. CZ2HF may be a potential agent for the treatment of AD.

Monitoring residue levels and dietary risk assessment of pymetrozine for Chinese consumption of cauliflower.

The present study investigates the occurrence of pymetrozine residues in cauliflower samples obtained from six cauliflower-producing areas of China during fixed time periods in 2017 and estimates the dietary risk of pymetrozine in cauliflower. A liquid chromatography with tandem mass spectrometry method was developed and validated to detect pymetrozine in cauliflower. The samples were extracted using 20 mL of acetonitrile and purified with dispersive solid-phase extraction using C18 as sorbent. The limit of quantification of pymetrozine was 0.008 mg/kg in cauliflower. The recoveries of the analyte were 82.04-95.18% with RSD <8.45%. The calibration curves for pymetrozine showed good linearities in the concentration range 0.004-2.0 mg/L with determination coefficients (R2 ) >0.999. Pymetrozine dissipated rapidly in cauliflower with a half-life of <4 days. The terminal residues of pymetrozine were <0.008-0.0881 mg/kg in cauliflower at 7, 10 and 14 days after spraying from six sites. The routine washing process removed about half amount of the pymetrozine in cauliflower; the reduction ratios were 51.0-52.8%. The dietary risk assessment indicated that pymetrozine did not exhibit obvious dietary health risks in cauliflower when good agricultural practices were implemented.

Icariside II ameliorates ibotenic acid-induced cognitive impairment and apoptotic response via modulation of MAPK pathway in rats.

BACKGROUND: Excitotoxicity is extensively recognized as a major pathological process of neuronal death and has been proved to play a key role in Alzheimer's disease (AD). ICS II, a flavonoid compound from Herba Epimedii Maxim, is attracting great interests due to its neuroprotective properties. PURPOSE: The present study was aimed to explore the effects of ICS II on cognitive dysfunction and apoptotic response induced by excitatory neurotoxin ibotenic acid (IBO) injection in rats. METHODS: Rats subjected to bilateral hippocampal injection of IBO were intragastrically administered with 4, 8 and 16 mg/kg ICS II or 0.6 mg/kg donepezil once a day for continuous 20 days. Learning and memory functions were tested by Morris water maze. The neuronal morphology in hippocampus was examined by HE staining and Nissl staining, respectively. Neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. The expression of apoptosis-related proteins and the activation of mitogen-activated protein kinase (MAPK) pathway were detected by Western blot. RESULTS: It was uncovered that hippocampal injection of IBO caused learning and memory impairment, neuronal damage and loss, as well as pro-apoptotic response. ICS II administrated at doses of 8 and 16 mg/kg not only rescued behavioral performance, but also protected hippocampal neurons against neurotoxicity via suppressing the elevation of Bax/Bcl-2 ratio and the activation of caspase-3. Meanwhile, ICS II repressed the down-regulation of calbindin protein induced by IBO. Additionally, ICS II exerted an inhibitory effect on MAPK (p38, ERK1/2 and JNK) pathway phosphorylation. CONCLUSION: These results suggest that ICS II attenuates IBO-induced cognitive deficits, possibly via the regulation of calbindin expression and the inhibition of apoptotic response. In addition, the MAPK signaling pathway is implicated in the potential mechanisms of ICS II against IBO-induced excitotoxicity, indicating that ICS II is a promising compound for treatment of excitotoxicity-related diseases, including AD.

Residual level of dimethachlon in rice-paddy field system and cooked rice determined by gas chromatography with electron capture detector.

In this study, a modified quick, easy, cheap, effective, rugged and safe method coupled with gas chromatography with electron capture detection was established to determine dimethachlon residues in paddy soil, rice husk, rice straw, brown rice and cooked rice. The limits of quantification of dimethachlon were 0.01 mg/kg for paddy soil, brown rice and cooked rice and 0.02 mg/kg for rice straw and rice husk. The mean recoveries were in the range 78.59-104.7% with relative standard deviation values of <10% for dimethachlon in the five matrices. For field experiments, the final residues of dimethachlon in paddy soil were < 0.05 mg/kg and were < 1.21 mg/kg in rice straw from six sites. The final residues of dimethachlon in the brown rice at 21, 28 and 35 days after spraying from six sites were 0.08-7.58 mg/kg, and 0.16-30.1 mg/kg in rice husk. Our six test sites covered the main rice-producing areas of China. The routine rice cooking process of a Chinese family could apparently increase the removal of dimethachlon in rice compared with brown rice, and the reduction ratios were > 96%.

Icariside II, a Broad-Spectrum Anti-cancer Agent, Reverses Beta-Amyloid-Induced Cognitive Impairment through Reducing Inflammation and Apoptosis in Rats.

Beta-amyloid (Aß) deposition, associated neuronal apoptosis and neuroinflammation are considered as the important factors which lead to cognitive deficits in Alzheimer's disease (AD). Icariside II (ICS II), an active flavonoid compound derived from Epimedium brevicornum Maxim, has been extensively used to treat erectile dysfunction, osteoporosis and dementia in traditional Chinese medicine. Recently, ICS II attracts great interest due to its broad-spectrum anti-cancer property. ICS II shows an anti-inflammatory potential both in cancer treatment and cerebral ischemia-reperfusion. It is not yet clear whether the anti-inflammatory effect of ICS II could delay progression of AD. Therefore, the current study aimed to investigate the effects of ICS II on the behavioral deficits, Aß levels, neuroinflammatory responses and apoptosis in Aß25-35-treated rats. We found that bilateral hippocampal injection of Aß25-35 induced cognitive impairment, neuronal damage, along with increase of Aß, inflammation and apoptosis in hippocampus of rats. However, treatment with ICS II 20 mg/kg could improve the cognitive deficits, ameliorate neuronal death, and reduce the levels of Aß in the hippocampus. Furthermore, ICS II could suppress microglial and astrocytic activation, inhibit expression of IL-1ß, TNF-α, COX-2, and iNOS mRNA and protein, and attenuate the Aß induced Bax/Bcl-2 ratio elevation and caspase-3 activation. In conclusion, these results showed that ICS II could reverse Aß-induced cognitive deficits, possibly via the inhibition of neuroinflammation and apoptosis, which suggested a potential protective effect of ICS II on AD.

[Characterization of Vibrio parahaemolyticus obtained from environment and cases of foodborne disease in Shenzhen, during 2006 - 2008].

OBJECTIVE: To analyze the serological and genetic divergence in the Vibrio parahaemolyticus from environment and cases of foodborne disease, and to compare these two groups in terms of virulence and other biological traits. METHODS: Serotyping, multi-PCR, and pulse-field gel electrophoresis (PFGE) were carried out. RESULTS: The main serotypes of cases isolates were O3:K6 (40.8%), O1: KUT (7.1%), O4:K8 (7.1%), and the main serotypes of environmental isolates were O3:KUT (14.2%), O1: KUT (11.4%) and O2:K3 (11.4%). No O3:K6 strain was isolated from environment. Most cases isolates were tdh positive and trh negative, which account for 83.7%, while most environmental isolates were tdh negative and trh negative, which account for 88.6%. PFGE indicated that Clone P1 was the dominant clone cluster, including serotype O3: K6 (29 isolates), O4: K68 (4 isolates), O11: K36 (3 isolates), O1: K25 (2 isolates), and these strains were all obtained from cases of foodborne disease. No dominant clone cluster was found in environmental isolates. CONCLUSIONS: V. parahaemolyticus from cases of foodborne disease in Shenzhen mostly were hemolytic, tdh positive and trh negative, there were dominant PFGE type in cases isolates, the main serotype was O3:K6, while environmental isolates mostly were non-hemolytic, tdh negative and trh negative, no dominant PFGE type was found.