Notoginsenoside R1 promotes Lgr5+ stem cell and epithelium renovation in colitis mice via activating Wnt/ß-Catenin signaling.

Inflammatory bowel disease (IBD) is characterized by persistent damage to the intestinal barrier and excessive inflammation, leading to increased intestinal permeability. Current treatments of IBD primarily address inflammation, neglecting epithelial repair. Our previous study has reported the therapeutic potential of notoginsenoside R1 (NGR1), a characteristic saponin from the root of Panax notoginseng, in alleviating acute colitis by reducing mucosal inflammation. In this study we investigated the reparative effects of NGR1 on mucosal barrier damage after the acute injury stage of DSS exposure. DSS-induced colitis mice were orally treated with NGR1 (25, 50, 125 mg·kg-1·d-1) for 10 days. Body weight and rectal bleeding were daily monitored throughout the experiment, then mice were euthanized, and the colon was collected for analysis. We showed that NGR1 administration dose-dependently ameliorated mucosal inflammation and enhanced epithelial repair evidenced by increased tight junction proteins, mucus production and reduced permeability in colitis mice. We then performed transcriptomic analysis on rectal tissue using RNA-sequencing, and found NGR1 administration stimulated the proliferation of intestinal crypt cells and facilitated the repair of epithelial injury; NGR1 upregulated ISC marker Lgr5, the genes for differentiation of intestinal stem cells (ISCs), as well as BrdU incorporation in crypts of colitis mice. In NCM460 human intestinal epithelial cells in vitro, treatment with NGR1 (100 µM) promoted wound healing and reduced cell apoptosis. NGR1 (100 µM) also increased Lgr5+ cells and budding rates in a 3D intestinal organoid model. We demonstrated that NGR1 promoted ISC proliferation and differentiation through activation of the Wnt signaling pathway. Co-treatment with Wnt inhibitor ICG-001 partially counteracted the effects of NGR1 on crypt Lgr5+ ISCs, organoid budding rates, and overall mice colitis improvement. These results suggest that NGR1 alleviates DSS-induced colitis in mice by promoting the regeneration of Lgr5+ stem cells and intestinal reconstruction, at least partially via activation of the Wnt/ß-Catenin signaling pathway. Schematic diagram of the mechanism of NGR1 in alleviating colitis. DSS caused widespread mucosal inflammation epithelial injury. This was manifested by the decreased expression of tight junction proteins, reduced mucus production in goblet cells, and increased intestinal permeability in colitis mice. Additionally, Lgr5+ ISCs were in obviously deficiency in colitis mice, with aberrant down-regulation of the Wnt/ß-Catenin signaling. However, NGR1 amplified the expression of the ISC marker Lgr5, elevated the expression of genes associated with ISC differentiation, enhanced the incorporation of BrdU in the crypt and promoted epithelial restoration to alleviate DSS-induced colitis in mice, at least partially, by activating the Wnt/ß-Catenin signaling pathway.

Vof16-miR-185-5p-GAP43 network improves the outcomes following spinal cord injury via enhancing self-repair and promoting axonal growth.

INTRODUCTION: Self-repair of spinal cord injury (SCI) has been found in humans and experimental animals with partial recovery of neurological functions. However, the regulatory mechanisms underlying the spontaneous locomotion recovery after SCI are elusive. AIMS: This study was aimed at evaluating the pathological changes in injured spinal cord and exploring the possible mechanism related to the spontaneous recovery. RESULTS: Immunofluorescence staining was performed to detect GAP43 expression in lesion site after spinal cord transection (SCT) in rats. Then RNA sequencing and gene ontology (GO) analysis were employed to predict lncRNA that correlates with GAP43. LncRNA smart-silencing was applied to verify the function of lncRNA vof16 in vitro, and knockout rats were used to evaluate its role in neurobehavioral functions after SCT. MicroRNA sequencing, target scan, and RNA22 prediction were performed to further explore the underlying regulatory mechanisms, and miR-185-5p stands out. A miR-185-5p site-regulated relationship with GAP43 and vof16 was determined by luciferase activity analysis. GAP43-silencing, miR-185-5p-mimic/inhibitor, and miR-185-5p knockout rats were also applied to elucidate their effects on spinal cord neurite growth and neurobehavioral function after SCT. We found that a time-dependent increase of GAP43 corresponded with the limited neurological recovery in rats with SCT. CRNA chip and GO analysis revealed lncRNA vof16 was the most functional in targeting GAP43 in SCT rats. Additionally, silencing vof16 suppressed neurite growth and attenuated the motor dysfunction in SCT rats. Luciferase reporter assay showed that miR-185-5p competitively bound the same regulatory region of vof16 and GAP43. CONCLUSIONS: Our data indicated miR-185-5p could be a detrimental factor in SCT, and vof16 may function as a ceRNA by competitively binding miR-185-5p to modulate GAP43 in the process of self-recovery after SCT. Our study revealed a novel vof16-miR-185-5p-GAP43 regulatory network in neurological self-repair after SCT and may underlie the potential treatment target for SCI.

Dietary pattern interfered with the impacts of pesticide exposure by regulating the bioavailability and gut microbiota.

Dietary intake is an essential way for pesticides to enter the human body. The effects of dietary pattern on the risks of pesticides and what diet can reduce the damage are largely unknown. Here, it is found that Mediterranean diet and Vegetarian diet could alleviate insulin resistance and obesity induced by chlorpyrifos, while Western diet could aggravate that. Gut microbiota and chlorpyrifos bioavailability mediated by the diets were involved in these effects. Both the dietary pattern and chlorpyrifos could change the composition of gut microbiota. Chlorpyrifos caused gut dysbacteriosis which was an important reason for the induced metabolic syndrome. Mediterranean diet and Vegetarian diet could maintain gut microbiota homeostasis and increase intestinal bacteria producing short-chain fatty acids, repair the gut microbiota and intestinal barrier damaged by chlorpyrifos. High dietary fat intake increased the bioavailability of chlorpyrifos, which aggravated the gut dysbacteriosis and destruction of intestinal integrity. Thus, the amount of endotoxin entering the blood increased and caused low-grade inflammation, which was also an important pathway of metabolic syndrome. The results suggested that although it was almost impossible to avoid the exposure to pesticides in modern life, healthy diets could regulate beneficial gut microbiota and alleviate the risk of pesticide exposure.

Immune-related lncRNAs, LINC01268 and CTB-31O20.2, as favorable prognostic markers for glioma inhibition.

Background: Glioblastoma (GBM) is the most common and fatal tumor in the central nervous system. Recent studies have found that long non-coding RNAs (lncRNAs) serve as competitive endogenous RNAs (ceRNAs) and play an important role in GBM by regulating immune responses. The aim of the present study was to identify lncRNAs with immune relevance and functions in GBM. Methods: We analyzed GBM datasets from The Cancer Genome Atlas (TCGA) database to obtain 356 significantly differentially expressed lncRNAs (DE-lncRNAs), 4,951 DE-mRNAs, and 34 DE-miRNAs in GBM, respectively. For mRNAs, 369 DE-mRNAs were identified as immune-related genes in the ImmPort database. For DE-lncRNAs, univariate analysis identified 39 DE-lncRNAs with prognostic significance, and 9 DE-lncRNAs were included in the ImmLnc database. Combined analysis was then conducted by integrating 9 immune-related DE-lncRNAs, 369 immune-related DE-mRNAs, and 34 DE-miRNAs. A ceRNA network composed of 2 upregulated lncRNAs (LINC01268 and CTB-31O20.2), 3 downregulated miRNAs, and 5 upregulated mRNAs was generated. Results: Kaplan-Meier survival analysis and univariate and multivariate Cox regression analyses showed that LINC01268 and CTB-31O20.2 serve as independent favorable prognostic markers in GBM. LINC01268 and CTB-31O20.2 overexpression was conducted in GBM cell U251. Cell Counting Kit-8 (CCK8), Transwell assay, and scratch healing assay indicated that LINC01268 and CTB-31O20.2 inhibit GBM cell line, U251, proliferation, invasion, and migration. Conclusions: LINC01268 and CTB-31O20.2 are independent prognostic immune-related markers, and reduce cancer cell proliferation and metastasis in GBM.

Effect of Sutellarin on Neurogenesis in Neonatal Hypoxia-Ischemia Rat Model: Potential Mechanisms of Action.

To investigate the therapeutic efficacy of Scutellarin (SCU) on neurite growth and neurological functional recovery in neonatal hypoxic-ischemic (HI) rats. Primary cortical neurons were cultured to detect the effect of SCU on cell viability of neurons under oxygen-glucose deprivation (OGD). Double immunofluorescence staining of Tuj1 and TUNEL then observed the neurite growth and cell apoptosis in vitro,and double immunofluorescence staining of NEUN and TUNEL was performed to examine the neuronal apoptosis and cell apoptosis in brain tissues after HI in vivo. Pharmacological efficacy of SCU was also evaluated in HI rats by neurobehavioral tests, triphenyl tetrazolium chloride staining, Hematoxylin and eosin staining and Nissl staining. Astrocytes and microglia expression in damaged brain tissues were detected by immunostaining of GFAP and Iba1. A quantitative real-time polymerase chain reaction and western blot were applied to investigate the genetic expression changes and the protein levels of autophagy-related proteins in the injured cortex and hippocampus after HI. We found that SCU administration preserved cell viability, promoted neurite outgrowth and suppressed apoptosis of neurons subjected to OGD both in vitroand in vivo. Meanwhile, 20 mg/kg SCU treatment improved neurological functions and decreased the expression of astrocytes and microglia in the cortex and hippocampus of HI rats. Additionally, SCU treatment depressed the elevated levels of autophagy-related proteins and the p75 neurotrophin receptor (p75NTR) in both cortex and hippocampus. This study demonstrated the potential therapeutic efficacy of SCU by enhancing neurogenesis and restoring long-term neurological dysfunctions, which might be associated with p75NTR depletion in HI rats.

Prognostic significance of high triglyceride and apolipoprotein B levels in patients with stage III and high-risk stage II colorectal cancer undergoing curative surgery.

Although epidemiologic studies suggest that dyslipidemia increases the risk of colorectal cancer (CRC), the prognostic value of blood lipid and apolipoprotein levels in CRC remains unclear. The aim of the present study was to investigate the impact of blood lipid and apolipoprotein levels on the prognosis of patients with stage III and high-risk stage II CRC undergoing curative surgery. Preoperative levels of total cholesterol, triglycerides (TG), high-density lipoprotein, low-density lipoprotein, very-low-density lipoprotein, apolipoprotein A1 and apolipoprotein B (APO-B) in patients with CRC undergoing surgery were evaluated. The cut-off values of these factors were determined by the maximal x2 method and were used to classify patients into two prognostic groups: Poor and good prognosis groups. The patients prognostic values were assessed using the Kaplan-Meier curve and Cox regression analysis. In addition, the impact of these parameters on the prognosis and their predictive accuracy were evaluated using nomograms and Harrells concordance index, respectively. In total, 246 patients were included in this evaluation. Based on the cut-off points for TG (1.53 mmol/l in men and 1.58 mmol/l in women) and APO-B (0.73 mmol/l in men and women), the present study determined that both TG and APO-B were predictors of disease-free survival (DFS) and overall survival (OS). Multivariate analysis demonstrated that high TG (men, ≥1.53 mmol/l; women, ≥1.58 mmol/l) and high APO-B (≥0.73 mmol/l) levels were significantly associated with decreased DFS and OS. Nomograms that included values for TG and APO-B levels demonstrated higher predictive accuracy compared with that of nomograms without these values. These results indicated that TG and APO-B levels may be good independent prognostic biomarkers after radical CRC surgery. Therefore, adjusting these parameters to moderate levels may be beneficial.

The Combination of Adipose-derived Schwann-like Cells and Acellular Nerve Allografts Promotes Sciatic Nerve Regeneration and Repair through the JAK2/STAT3 Signaling Pathway in Rats.

Schwann cells (SCs) combined with acellular nerve allografts (ANAs) effectively promote the regeneration and repair of peripheral nerves, but the exact mechanism has not been fully elucidated. However, the disadvantages of SCs include their limited source and slow rate of expansion in vitro. Previous studies have found that adipose-derived stem cells have the ability to differentiate into Schwann-like cells. Therefore, we speculated that Schwann-like cells combined with ANAs could profoundly facilitate nerve regeneration and repair. The aim of the present study was to investigate the cellular and molecular mechanisms of regeneration and repair. In this study, tissue-engineered nerves were first constructed by adipose-derived Schwann-like cells and ANAs to bridge missing sciatic nerves. Then, the rats were randomly divided into five groups (n = 12 per group): a Control group; a Model group; an ADSC group; an SC-L group; and a DMEM group. Twelve weeks postsurgery, behavioral function tests and molecular biological techniques were used to evaluate the function of regenerated nerves and the relevant molecular mechanisms after sciatic nerve injury (SNI). The results showed that adipose-derived Schwann-like cells combined with ANAs markedly promoted sciatic nerve regeneration and repair. These findings also demonstrated that the expression of neurotrophic factors (NFs) was increased, and the expression of Janus activated kinase2 (JAK2)/P-JAK2, signal transducer and activator of transcription-3 (STAT3)/P-STAT3 was decreased in the spinal cord after SNI. Therefore, these results suggested that highly expressed NFs in the spinal cord could promote nerve regeneration and repair by inhibiting activation of the JAK2/STAT3 signaling pathway.

GLTSCR1, ATM, PPP1R13L and CD3EAP Genetic Variants and Lung Cancer Risk in a Chinese Population.

Genetic variants in glioma tumor suppressor candidate region gene 1 (GLTSCR1) and ATM serine/threonine kinase (ATM) have been associated with various cancer risks. Epidemiological studies also revealed the association of variants of GLTSCR1 and ATM genes with different brain tumors. However, little is known about the relationship between both gene polymorphisms and lung cancer risk. We conducted a Chinese hospital-based casecontrol study involving 384 lung cancer cases and 387 cancer-free controls. No significant differences in the single polymorphism (GLTSCR1 rs1035938 and ATM rs11212592) association were found in five genetic models (co-dominant, dominant, recessive, overdominant and log-additive models) (adjusted by smoking duration). Join effect of three SNPs (PPP1R13L rs1970764, CD3EAP rs967591, GLTSCR1 rs1035938) on chromosome 19q13.3 showed that the designated haplotype8 (rs 1970764G-rs967591A-rs1035938C) [OR (95% CI)=1.60(1.11-2.32), P/0.012] andhaplotype8 (rs1970764G-rs967591G-rs1035938T) [OR (95% CI)=2.45 (1.17-5.12), P=0.018] were associated with increased risk of lung cancer (adjusted by smoking duration). The analysis of multifactor dimensionality reduction revealed that two 3-way models were the best fit models in analyses of 2 loci (P<0.001) or 4 loci (Р=0.015-0.016). The entropy-based analysis indicated the strongest synergistic effect between PPP1R13L rs1970764 and ATM rs11212592 in analysis of four genes. In conclusion, our study suggests that haplotypes consisting of PPP1R13L rs1970764-CD3EAP rs961591-GLTSCR1 rs1035938 on Chr19q13.3, interaction of smoking and GLTSCR1 rs1035938-ATM rs11212592, and synergistic action of PPP1R13L rs1970764 and ATM rs11212592 may associate with lung cancer risk in the Chinese population.

Glycation of high-density lipoprotein triggers oxidative stress and promotes the proliferation and migration of vascular smooth muscle cells.

BACKGROUND: In type 2 diabetes mellitus (T2DM), high-density lipoprotein (HDL) impairs its anti-atherogenic properties and even develops to a pro-inflammatory and pro-atherogenic phenotype because of abnormal compositions and modifications. In this study, we examined the effects and the related mechanisms of glycation of HDL on the proliferation and migration of vascular smooth muscle cells (VSMCs). METHODS & RESULTS: Glycated HDL (G-HDL) was modified with D-glucose (25 mmol/L) in vitro. Diabetic HDL (D-HDL) was isolated from T2DM patients. Rat VSMCs were isolated from the thoracic aortas. Human VSMCs were obtained from ScienCell Research Laboratories. Alpha-actin was detected through immunofluorescence. VSMC proliferation was assayed by Cell Count. VSMC migration was determined by transwell chamber and scratch-wound assay. Intracellular reactive oxygen species (ROS) was detected based on ROS-mediated 2',7'-dichlorofluorescein (DCFH-DA) fluorescence. Compared to native HDL (N-HDL), G-HDL remarkably promoted VSMC proliferation and migration in the dose and time-dependent manners. In addition, G-HDL enhanced ROS generation in VSMCs. However, the ROS scavenger, N-acetylcysteine, efficiently decreased ROS production and subsequently inhibited the proliferation of VSMCs induced by G-HDL. Similarly, D-HDL from T2DM patients also promoted ROS release and VSMC proliferation and migration. CONCLUSIONS: HDL either glycated in vitro or isolated from T2DM patients triggered VSMC proliferation, migration, and oxidative stress. These results might partly interpret the higher morbidity of cardiovascular disease in T2DM patients.

Environmental behavior of the chiral insecticide fipronil: Enantioselective toxicity, distribution and transformation in aquatic ecosystem.

The enantioselective environmental behaviors of the chiral insecticide fipronil and its metabolites in lab-scale aquatic ecosystems were studied and the toxicity of fipronil enantiomers and the metabolites to non-target organisms Lemna minor (L. minor) and Anodonta woodiana (A. woodiana) was also investigated in this work. Water-sediment, water-L. minor, water-A. woodiana, and water-sediment-L. minor-A. woodiana ecosystems were set up and exposed to fipronil through a 90-day period. The results showed fipronil could be degraded significantly faster (half-life of 4.6 days) in the complex water-sediment-L. minor-A. woodiana ecosystem. A. woodiana played a crucial role in the dissipation of fipronil, and the microorganisms in the sediment also made great contribution to the degradation of fipronil in aquatic ecosystems. All the three metabolites fipronil desulfinyl, fipronil sulfide and fipronil sulfone were detected in the ecosystems and were more persistent than fipronil. Enantioselective degradation of fipronil was observed with S-fipronil being preferentially degraded in sediment and L. minor, while R-fipronil was metabolized preferentially in A. woodiana. EC50 for L. minor was obtained using 7-day exposure, and for A. woodiana was obtained using 72-h exposure. S-fipronil was more toxic to A. woodiana, while R-fipronil showed higher toxicity to L. minor. Moreover, the three metabolites were found more toxic than fipronil indicating significant environment risks due to their persistence. The present study might have important implications for the risk assessment of fipronil and its metabolites in real aquatic environment.

The toxicity, bioaccumulation, elimination, conversion of the enantiomers of fipronil in Anodonta woodiana.

The enantioselective bioaccumulation and elimination of fipronil in Anodonta woodiana (A. woodiana) were studied and the main metabolites fipronil desulfinyl, fipronil sulfide and fipronil sulfone were determined. The acute toxicity of the enantiomers of fipronil and the three metabolites were also investigated. In the bioaccumulation process, fipronil in A. woodiana reached equilibrium after 11days with BCF value of 0.2, and the enantiomeric fraction (EF) values showed that the bioaccumulation was enantioselective with enantioenrichment of S-fipronil. The degradation of fipronil in A. woodiana fitted first-order kinetics model with half-lives of the enantiomers were 5.8 d for R-fipronil and 7.6 d for S-fipronil, and the EF values decreasing from 0.5 gradually indicating the R-enantiomer was preferentially degraded. The degradation of single enantiomers was also performed and the results revealed a fast conversion of R-fipronil to S-fipronil by A. woodiana. The three metabolites were all detected in A. woodiana-water system, in which fipronil sulfone and fipronil sulfide had higher concentration levels. According to the 72-h LC50 values, S-fipronil was much more toxic than the racemate and R-fipronil. Moreover, the metabolites were more toxic than the parent fipronil. The results suggested the individual enantiomers of chiral pollutants and the metabolites should be considered in the risk assessments.

[Systematic report on re-evaluating kudiezi injection].

There are few articles or reports collecting evidence about Kudiezi injection from premarketing and postmarketing research or studies systematically. This article is an exact miniature of a systematical report about Kudiezi injection. We analyzed information from four aspects, such as quality control reports, non-clinical premarketing safety experiments, postmarketing research (efficacy studies, hospital information system data and national spontaneous reporting system data), and literature analysis. All the four aspects build an evidence body for Kudiezi injection in order to inform its safety use in clinical practice and further study.

Enantioselective toxicity and degradation of the chiral insecticide fipronil in Scenedesmus obliguus suspension system.

Fipronil is an effective insecticide, but it presents highly toxic effects in nontarget aquatic organisms. The present study examined the enantioselective toxicity and degradation of fipronil enantiomers in a freshwater algae Scenedesmus obliguus suspension. There was a substantial difference in the acute toxicity of the enantiomers to S. obliguus, with 72-h median effective concentrations (EC50s) of 0.29 mg L(-1) and 1.50 mg L(-1) for the R-fipronil and S-fipronil, respectively. The influences on the concentration of chlorophyll a, chlorophyll b, and carotenoids were determined, and the effects of fipronil on the concentration of chlorophyll a and chlorophyll b were also enantioselective. The degradation of fipronil in algae suspension was enantioselective, with half-lives for R-fipronil and S-fipronil of 2.9 d and 3.2 d, respectively, and the enantiomer fraction reaching 0.65 at the day 17. The enantiomeric differences should be taken into consideration for fipronil risk assessment.

Enantioselective toxicity, bioaccumulation and degradation of the chiral insecticide fipronil in earthworms (Eisenia feotida).

The enantioselective acute toxicity to earthworms of racemic fipronil and its individual enantiomers was studied. R-(-)-fipronil was approximately 1.5 times more toxic than the racemate and approximately 2 times more toxic than S-(+)-fipronil after 72 and 96 h of exposure, respectively. Assays of fipronil enantiomer bioaccumulation and degradation in earthworms were conducted. The bio-concentration factors (BCFs) were slightly different between the two enantiomers. The enantiomeric fraction (EF) values in earthworms in the bioaccumulation period were approximately 0.5, which indicated there was no enantioselective bioaccumulation. In contrast, the degradation of fipronil in earthworms was enantioselective: the t1/2 values for R- and S-fipronil were 3.3 and 2.5 days, respectively, in natural soil, and 2.1 and 1.4 days, respectively, in artificial soil. The results of soil analyses showed that the degradation of fipronil was not enantioselective, which suggested that the enantioselectivity of fipronil in earthworms results from the organism's metabolism. The study also demonstrated that the presence of earthworms could accelerate the degradation of fipronil in soil.

ß-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in asenescence-accelerated prone 8 mice.

ß-Asarone is an active component of the Acori graminei rhizome that is a traditional Chinese medicine clinically used in treating dementia in China. However, the cognitive effect of ß-asarone and its mechanism has remained elusive. Here, we used asenescence-accelerated prone 8 (SAMP8) mice, which mimic many of the salient features of Alzheimer׳s disease (AD), to further investigate whether modulation of the ROCK signaling pathway and/or autophagy, synaptic loss is involved in the effects of ß-asarone on learning and memory. SAMP8 mice at the age of 6 months were intragastrically administered by ß-asarone or a vehicle daily for 2 months. Senescence-accelerated-resistant (SAMR1) mice were used as the control. Our results demonstrate that autophagy and ROCK expression were increased significantly in 8 months SAMP8 mice, which were concomitant with that SAMP8 mice at the same age displayed a significant synaptic loss and cognitive deficits. The up-regulation of ROCK expression and autophage in the hippocampus of SAMP8 were significantly reduced by ß-asarone, and prevents synaptic loss and improved cognitive function of the SAMP8 mice. ß-asarone decreased neuronophagia and lipofuscin in the hippocampus of SAMP8 mice, but did not reduce Aß42 levels and malondialdehyde levels and superoxide dismutase activities. Moreover, suppression of ROCK2 by siRNA significantly reduced the effects of ß-asarone on the autophage and synaptic proteins expression in PC12 cells damage induced by Aß1-40. Taken together, ß-asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice.

Development of a home-made extraction device for vortex-assisted surfactant-enhanced-emulsification liquid-liquid microextraction with lighter than water organic solvents.

We have developed a novel vortex-assisted surfactant-enhanced-emulsification liquid-liquid microextraction using the low density solvent for the determination of eight organophosphorus pesticides (OPPs) in water samples. The key point of this method is the application of a special home-made extraction device. The influence parameters relevant to this method were systemically investigated and the optimum conditions were as follow: 35µL of toluene was used as extraction solvent and 0.2mmol L-1 Triton X-100 was chosen as the surfactant to enhance the emulsification. Under the optimum experimental conditions, the limit of detections (LODs) of the method was ranged between 0.01 and 0.05µgL(-1) and the relative standard deviations (RSDs) were 2.9-8.1%. The calibration curve was linear in the range of 0.1-50.0µgL(-1), with the correlation coefficients (r) varying from 0.9949 to 0.9991. Finally, the developed method has been successfully applied to the determination of eight organophosphorus pesticides in river, reservoir and well water samples with recoveries between 82.1% and 98.7%.

Low-density solvent-based vortex-assisted surfactant-enhanced emulsification liquid-liquid microextraction and its application.

For the first time, the low-density solvent-based vortex-assisted surfactant-enhanced emulsification liquid-liquid microextraction, followed by GC-flame photometric detection has been developed for the determination of eight organophosphorus pesticides in aqueous samples. A small volume of organic extraction solvent (toluene) was dispersed into the aqueous samples by the assistance of surfactant and vortex agitator. The extraction was performed in a special disposable polyethylene pipette, allowing using the reagents with lower density than water as extraction solvents. The influence parameters were systemically investigated and optimized: toluene (30 µL) and Triton X-100 (0.2 mmol/L) were used as the extraction solvent and the surfactant, respectively, and the extraction was performed for 1 min under room temperature without adding sodium chloride. Under the optimum conditions, the validation parameters such as the RSD (n = 6; 2.1-11.3%), LOD (0.005 and 0.05 µg/L), and linear range (0.1-50.0 µg/L with correlation coefficients (0.9958-0.9992) showed the method was satisfying. The proposed method has been successfully applied to the determination of the organophosphorus pesticides in real samples with recoveries between 82.8 and 100.2%.

Characterization of phloroglucinol derivatives and diterpenes in Euphorbia ebracteolata Hayata by utilizing ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry.

Euphorbia ebracteolata Hayata (E. ebracteolata) is a Chinese herbal medicine used for the treatment of tumor diseases. An ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) based chemical profiling approach was established for the rapid separation and characterization on phloroglucinol derivatives and diterpenes in E. ebracteolata. Three phloroglucinol derivatives and nine diterpenes were identified by exact mass measurement and were further confirmed by Ms2 data. In addition, the chemical profiles of six compounds were acquired by reference standards. Furthermore, the fragmentation rules of phloroglucinol derivatives and diterpenes of E. ebracteolata were analyzed, and each chromatographic peak was classified.