Urine metabolomic characteristics of female patients with occupational chronic cadmium poisoning after 15 years of treatment.

Occupational chronic cadmium poisoning (OCCP) can cause irreversible organ damage. Currently, no effective treatment is available for OCCP, and effective and sensitive biomarkers for treatment evaluation are still lacking. In this study, metabolomics techniques were used to analyze changes in endogenous metabolites in the urine of patients with OCCP after 15 years of treatment. Thirty urine samples from female patients with OCCP and healthy female controls (n = 15 per group) were assessed using gas chromatography-time-of-flight mass spectrometry and ultra-high-performance liquid chromatography-Q-Exactive mass spectrometry. The OCCP group had higher concentrations of blood urea nitrogen and urinary cadmium but near-normal urinary concentrations of ß2 -microglobulin and retinol-binding protein. Compared with the control group, the OCCP group had 66 significantly different metabolites with a variable importance in projection score >1 and p < 0.05. These differential metabolites were involved in various metabolic pathways, such as creatine metabolism, nicotinate and nicotinamide metabolism, the pentose phosphate pathway, d-glutamine and d-glutamate metabolism, and amino acid metabolism. Compared with the control group, the OCCP group had significantly higher urinary concentrations of creatine, glutamic acid, quinolinic acid and nicotinic acid. In a receiver operator characteristic analysis, the area under the curve of creatine was higher than those for glutamic acid, quinolinic acid and nicotinic acid, indicating that urinary concentrations of creatine could be used as a sensitive biomarker for the diagnosis and prognosis of OCCP and for monitoring its treatment.

Involvement of m6A regulatory factor IGF2BP1 in malignant transformation of human bronchial epithelial Beas-2B cells induced by tobacco carcinogen NNK.

Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a Group 1 human carcinogen, as classified by the International Agency for Research of Cancer (IARC), and plays a significant role in lung carcinogenesis. However, its carcinogenic mechanism has not yet been fully elucidated. In this study, we performed colony formation assays, soft-agar assays, and tumor growth in nude mice to show that 100 mg/L NNK facilitates the malignant transformation of human bronchial epithelial Beas-2B cells. Transcriptome sequencing showed that insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), a post-transcriptional regulator, was differentially expressed in NNK-induced malignant transformed Beas-2B cells (2B-NNK cells). Small interfering RNA (SiRNA) was used to downregulate the expression of the IGF2BP1 gene. The reduction in protein expression, cell proliferation rate, and colony-forming ability and the increase in the apoptosis rate of Beas-2B cells transfected with the SiRNA indicated a role for IGF2BP1 in NNK-induced malignant transformation. IGF2BP1 is an N6-methyladenosine (m6A) regulatory factor, but it is not known whether its association with m6A mediates the malignant transformation of cells. Therefore, we measured the overall levels of m6A in Beas-2B cells. We found that the overall m6A level was lower in 2B-NNK cells, and knocking down IGF2BP1, the overall level of m6A was restored. Hence, we concluded that IGF2BP1 is involved in the NNK-induced malignant transformation of Beas-2B cells, possibly via m6A modification. This study therefore contributes novel insights into the environmental pathogenesis of lung cancer and the gene regulatory mechanisms of chemical carcinogenesis.

[Association of miR-146a rs2910164 G/C polymorphism with its abnormal expression and risk of gastric cancer].

OBJECTIVE: To assess the influence of rs2910164 G/C single nucleotide polymorphism (SNP) of the miR-146a gene on its expression and susceptibility to gastric cancer. METHODS: Fifty three gastric cancer patients and six gastric cancer cell lines were selected for determining the miR-146a expression by Taqman quantitative PCR. A model was constructed to assess the influence of miR-146a overexpression on the growth of AGS gastric cancer cells. A case-control study involving 417 gastric cancer patients and 420 cancer-free individuals was then conducted, and the allelic and genotypic frequencies of the rs2910164 G/C SNP were compared. The genotypes of all subjects were determined by using a Taqman allelic discrimination assay. A Taqman assay was also used to quantify mature and pri-miR-146a transcripts among 65 gastric cancer patients with known genotypes. RESULTS: The expression of miR-146a was down-regulated among the 53 gastric cancer patients and six gastric cancer cell lines. Over-expression of miR-146a has suppressed the growth of gastric cancer by inhibiting the G1/S-phase transition of AGS cells. The case-control study showed that subjects with GC/CC genotypes had significantly lower risk for gastric cancer compared with those with GG genotype. In addition, miR-146a G/C SNP has significantly increased the level of mature miR-146a in those with GC/CC genotype compared with GG genotype. CONCLUSION: Down-regulation of miR-146a may play an important role in the pathogenesis of gastric cancer. The rs2910164 polymorphism of the miR-146a gene may reduce the risk of gastric cancer by influencing the processing of mature miR-146a.

TROY interacts with Rho guanine nucleotide dissociation inhibitor α (RhoGDIα) to mediate Nogo-induced inhibition of neurite outgrowth.

TROY can functionally substitute p75 to comprise the Nogo receptor complex, which transduces the inhibitory signal of myelin-associated inhibitory factors on axon regeneration following CNS injury. The inhibition of neurite extension relies on TROY-dependent RhoA activation, but how TROY activates RhoA remains unclear. Here, we firstly identified Rho guanine nucleotide dissociation inhibitor α (RhoGDIα) as a binding partner of TROY using GST pull-down combined with two-dimensional gel electrophoresis and mass spectra analysis. The interaction was further confirmed by coimmunoprecipitation in vitro and in vivo. Deletion mutagenesis revealed that two regions of the TROY intracellular domain (amino acids 234-256 and 321-350) were essential for the interaction with RhoGDIα. Secondly, TROY and RhoGDIα were coexpressed in postnatal dorsal root ganglion neurons, cortex neurons, and cerebellar granule neurons (CGNs). Thirdly, TROY/RhoGDIα association was potentiated by Nogo-66 and was independent of p75/RhoGDIα interaction. Fourthly, TROY/RhoGDIα interaction was still able to activate RhoA when p75 was deficient. Furthermore, RhoA activation was decreased dramatically when TROY was knocked down in p75-deficient CGNs cells. Finally, RhoGDIα overexpression abolished RhoA activation and following neurite outgrowth inhibition by Nogo-66 in both wild-type and p75-deficient CGNs. These results showed that the association of RhoGDIα with TROY contributed to TROY-dependent RhoA activation and neurite outgrowth inhibition after Nogo-66 stimulation.

Sex-specific associations of urinary mixed-metal concentrations with femoral bone mineral density among older people: an NHANES (2017-2020) analysis.

Background: Heavy metal exposure is an important cause of reduced bone mineral density (BMD). Epidemiological studies focusing on the effects of mixed heavy metal exposure on BMD in middle-aged and older people are scarce. In single-metal studies, men and women have shown distinct responses of BMD to environmental metal exposure. This study therefore aimed to elucidate the association between mixed heavy metal exposure and BMD and to investigate whether it is sex-specific. Methods: Data from the 2017-2020 National Health and Nutrition Examination Survey were selected for this cross-sectional study. The study used three statistical methods, i.e., linear regression, Bayesian kernel machine regression (BKMR) modeling, and weighted quartiles (WQS) regression, to explore the association between the urinary concentrations of 11 metals (barium, cadmium, cobalt, cesium, manganese, molybdenum, lead, antimony, tin, thallium, and Tungsten), either individually or as a mixture, and total femoral BMD. Results: A total of 1,031 participants were included in this study. Femoral BMD was found to be higher in men than women. A significant negative correlation between the urinary concentrations of the 10 metals and femoral BMD was found in the overall cohort. Further gender sub-stratified analyses showed that in men, urinary metal concentrations were negatively correlated with femoral BMD, with cobalt and barium playing a significant and non-linear role in this effect. In women, although urinary metal concentrations negatively modulated femoral BMD, none of the correlations was statistically significant. Antimony showed sex-specific differences in its effect. Conclusion: The urinary concentrations of 10 mixed heavy metals were negatively correlated with femoral BMD in middle-aged and older participants, and this effect showed gender differences. These findings emphasize the differing role of mixed metal exposure in the process of BMD reduction between the sexes but require further validation by prospective studies.

Associations of occupational exposure to micro-LiNiCoMnO2 particles with systemic inflammation and cardiac dysfunction in cathode material production for lithium batteries.

Micro-LiNiCoMnO2 (MNCM), a cathode material with highest market share, has increasing demand with the growth of lithium battery industry. However, whether MNCM exposure brings adverse effects to workers remains unclear. This study aimed to explore the association between MNCM exposure with systemic inflammation and cardiac function. A cross-sectional study of 347 workers was undertaken from the MNCM production industry in Guangdong province, China in 2020. Metals in urine were measured using ICP-MS. The associations between metals, systemic inflammation, and cardiac function were appraised using a linear or logistic regression model. Bayesian kernel machine regression (BKMR) and generalized weighted quantile sum (gWQS) models were used to explore mixed metal exposures. The analysis of interaction and mediation was adopted to assess the role of inflammation in the relation between urinary metals and cardiac function. We observed that the levels of lithium (Li) and cobalt (Co) were positively associated with systemic inflammation and heart rate. The amount of Co contributed the highest weight on the increased systemic immune-inflammation index (SII) (59.8%), the system inflammation response index (SIRI) (44.3%), and heart rate (65.0%). Based on the mediation analysis, we estimated that SII mediated 32.3% and 20.9% of the associations between Li and Co with heart rate, and SIRI mediated 44.6% and 22.2% of the associations between Li and Co with heart rate, respectively. This study demonstrated for the first time that MNCM exposure increased the risk of workers' systemic inflammation and elevated heart rate, which were contributed by the excessive Li and Co exposure. Additionally, it indicates that systemic inflammation was a major mediator of the associations of Li and Co with cardiac function in MNCM production workers.

Slit2 regulates the dispersal of oligodendrocyte precursor cells via Fyn/RhoA signaling.

Oligodendrocyte precursor cells (OPCs) are a unique type of glia that are responsible for the myelination of the central nervous system. OPC migration is important for myelin formation during central nervous system development and repair. However, the precise extracellular and intracellular mechanisms that regulate OPC migration remain elusive. Slits were reported to regulate neurodevelopmental processes such as migration, adhesion, axon guidance, and elongation through binding to roundabout receptors (Robos). However, the potential roles of Slits/Robos in oligodendrocytes remain unknown. In this study, Slit2 was found to be involved in regulating the dispersal of OPCs through the association between Robo1 and Fyn. Initially, we examined the expression of Robos in OPCs both in vitro and in vivo. Subsequently, the Boyden chamber assay showed that Slit2 could inhibit OPC migration. RoboN, a specific inhibitor of Robos, could significantly attenuate this effect. The effects were confirmed through the explant migration assay. Furthermore, treating OPCs with Slit2 protein deactivated Fyn and increased the level of activated RhoA-GTP. Finally, Fyn was found to form complexes with Robo1, but this association was decreased after Slit2 stimulation. Thus, we demonstrate for the first time that Slit2 regulates the dispersal of oligodendrocyte precursor cells through Fyn and RhoA signaling.

Chimeric RNA RRM2-C2orf48 plays an oncogenic role in the development of NNK-induced lung cancer.

Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we reported that high-expressed chimeric RNA RRM2-C2orf48 was found in malignantly transformed BEAS-2B cells induced by 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK) in 74 lung cancer patients and several lung cancer cell lines. The expression level of RRM2-C2orf48 was significantly correlated with lymph node metastasis, distant metastasis, tumor-lymph node-metastasis (TNM) stage, and smoking. Overexpressing RRM2-C2orf48 promoted cell growth and accelerated the process of NNK-induced lung cancer. RRM2-C2orf48 knockdown inhibited the growth of RRM2-C2orf48-overexpressing BEAS-2B cells. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48 in lung cancer. In summary, chimeric RNA RRM2-C2orf48 accelerated the process of NNK-induced lung cancer, and miR-219a-2-3p may be involved in this process.

CircRNA hsa_circ_0000043 acts as a miR-4492 sponge to promote lung cancer progression via BDNF and STAT3 expression regulation in anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide-transformed 16HBE cells.

Increasing evidence shows that circular RNA (circRNA) plays an important role in the progression of lung cancer. In this study, we found that has_circ_0000043 was highly expressed in 16HBE-T human bronchial epithelial cells that were malignantly transformed by benzo[a]pyrene-trans-7,8-diol-9,10-epoxide via circRNA microarray. We verified that hsa_circ_0000043 was also significantly overexpressed in lung cancer cell lines and tissues. Moreover, hsa_circ_0000043 overexpression was positively correlated with poor clinicopathological parameters, such as tumor-node metastasis stage, distant metastasis, lymph-node metastasis, and overall survival. In vitro assays revealed that hsa_circ_0000043 inhibition suppressed 16HBE-T cell proliferation, migration, and invasion. Furthermore, hsa_circ_0000043 inhibition suppressed tumor growth in a mouse xenograft model. We discovered that hsa_circ_0000043 binds with miR-4492, acting as a miR-4492 sponge. Decreased miR-4492 expression was also associated with poor clinicopathological parameters. Thus, hsa_circ_0000043 was shown to contribute to the proliferation, malignant transformation ability, migration, and invasion of 16HBE-T cells via miR-4492 sponging and BDNF and STAT3 involvement.

A PVDF/g-C3N4-Based Composite Polymer Electrolytes for Sodium-Ion Battery.

As one of the most promising candidates for all-solid-state sodium-ion batteries and sodium-metal batteries, polyvinylidene difluoride (PVDF) and amorphous hexafluoropropylene (HFP) copolymerized polymer solid electrolytes still suffer from a relatively low room temperature ionic conductivity. To modify the properties of PVDF-HEP copolymer electrolytes, we introduce the graphitic C3N4 (g-C3N4) nanosheets as a novel nanofiller to form g-C3N4 composite solid polymer electrolytes (CSPEs). The analysis shows that the g-C3N4 filler can not only modify the structure in g-C3N4CSPEs by reducing the crystallinity, compared to the PVDF-HFP solid polymer electrolytes (SPEs), but also promote a further dissociation with the sodium salt through interaction between the surface atoms of the g-C3N4 and the sodium salt. As a result, enhanced electrical properties such as ionic conductivity, Na+ transference number, mechanical properties and thermal stability of the composite electrolyte can be observed. In particular, a low Na deposition/dissolution overpotential of about 100 mV at a current density of 1 mA cm-2 was found after 160 cycles with the incorporation of g-C3N4. By applying the g-C3N4 CSPEs in the sodium-metal battery with Na3V2(PO4)3 cathode, the coin cell battery exhibits a lower polarization voltage at 90 mV, and a stable reversible capacity of 93 mAh g-1 after 200 cycles at 1 C.

DNA adduct formation and reduced EIF4A3expression contributes to benzo[a]pyrene-induced DNA damage in human bronchial epithelial BEAS-2B cells.

Benzo[a]pyrene(B[a]P) is a known human carcinogen. The ability of B[a]P to form stable DNA adducts has been repeatedly demonstrated. However, the relationship between DNA adduct formation and cell damage and its underlying molecular mechanisms are less well understood. In this study, we determined the cytotoxicity of benzo[a]pyrenediolepoxide, a metabolite of B[a]P, in human bronchial epithelial cells (BEAS-2B). The formation of BPDE-DNA adducts was quantified using a dot blot. DNA damage resulting from the formation of BPDE-DNA adducts was detected by chromatin immuneprecipitation sequencing (ChIP-Seq), with minor modifications, using specific antibodies against BPDE. In total, 1846 differentially expressed gene loci were detected between the treatment and control groups. The distribution of the BPDE-bound regions indicated that BPDE could covalently bind with both coding and non-coding regions to cause DNA damage. However, the majority of binding occurred at protein-coding genes. Furthermore, among the BPDE-bound genes, we found 16 protein-coding genes related to DNA damage repair. We explored the response to BPDE exposure at the transcriptional level using qRT-PCR and observed a strong inhibition of EIF4A3. We then established an EIF4A3 overexpression cell model and performed comet assays, which revealed that the levels of DNA damage in EIF4A3-overexpressing cells were lower than those in normal cells following BPDE exposure. This suggests that the BPDE-DNA adduct-induced reduction in EIF4A3 expression contributed to the DNA damage induced by BPDE exposure in BEAS-2B cells. These novel findings indicate that ChIP-Seq combined with BPDE specific antibody may be used for exploring the underlying mechanism of DNA adduct-induced genomic damage.

Identification of SRXN1 and KRT6A as Key Genes in Smoking-Related Non-Small-Cell Lung Cancer Through Bioinformatics and Functional Analyses.

BACKGROUND: Lung cancer is the leading cause of cancer-related mortality worldwide. Although cigarette smoking is an established risk factor for lung cancer, few reliable smoking-related biomarkers for non-small-cell lung cancer (NSCLC) are available. An improved understanding of these biomarkers would further the development of new biomarker-targeted therapies and lead to improvements in overall patient survival. METHODS: We performed bioinformatic analysis to screened potential target genes, then quantitative PCR, western, siRNA, CCK-8, flow cytometry, tumorigenicity assays in nude mice were performed to validated the function. RESULTS: In this study, we identified 83 smoking-related genes (SRGs) based on an integration analysis of two Gene Expression Omnibus (GEO) datasets, and 27 hub SRGs with potential carcinogenic effects by analyzing a dataset of smokers with NSCLC in The Cancer Genome Atlas (TCGA) database. A survival analysis revealed three genes with potential prognostic value, namely SRXN1, KRT6A and JAKMIP3. A univariate Cox analysis revealed significant associations of elevated SRXN1 and KRT6A expression with prognosis. A receiver operating characteristic (ROC) curve analysis indicated the high diagnostic value of SRXN1 and KRT6A for smoking and cancer. Quantitative PCR and western blotting validated the increased expression of SRXN1 and KRT6A mRNA and protein, respectively, in lung cancer cell lines and NSCLC tissues. In patients with NSCLC, SRXN1 and KRT6A expression was associated with the tumor-node-metastasis (TNM) stage, presence of metastasis, history of smoking and daily smoking consumption. Furthermore, inhibition of SRXN1 or KRT6A suppressed viability and enhanced apoptosis in the A549 human lung carcinoma cell line. Tumorigenicity assays in nude mice confirmed that the siRNA-mediated downregulation of SRXN1 and KRT6A expression inhibited tumor growth in vivo. CONCLUSIONS: In summary, SRXN1 and KRT6A act as oncogenes in NSCLC and might be potential biomarkers of smoking exposure and the early diagnosis and prognosis of NSCLC in smokers, which is vital for lung cancer therapy.

A genome-wide screen for differentially methylated long noncoding RNAs identified that lncAC007255.8 is regulated by promoter DNA methylation in Beas-2B cells malignantly transformed by NNK.

Tobacco exposure is well known to induce genetic and epigenetic changes that contribute to the pathogenesis of lung cancer. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a significant tobacco-specific carcinogen, but the oncogenic mechanisms of NNK have not been thoroughly elucidated. In this study we found that DNA methyltransferase 1 (DNMT1) was overexpressed in malignantly transformed human bronchial epithelial Beas-2B cells induced by NNK (2B-NNK cells), by treatment with NNK (400 µg/mL) for 7 days. An Arraystar Human noncoding RNA Promoter Microarray was used to detect the DNA methylation status of the promoter region of long noncoding RNAs (lncRNAs). The result showed that 1010 differentially methylated fragments were present in the lncRNA promoter region. QRT-PCR revealed that the expression of lncRNA AC007255.8 was remarkably downregulated in 2B-NNK cells and lung cancer tissues. Furthermore, Methylation-specific PCR showed that the methylation of the lncRNA AC007255.8 promoter was increased in 2B-NNK cells and lung cancer tissues. The reduced expression of lncRNA AC007255.8 was significantly associated with hypermethylation of lncRNA AC007255.8 promoter region. LncRNA AC007255.8 overexpression could result in decreased cell proliferation and increased cell apoptosis in 2B-NNK cells. In conclusion, NNK induced lncRNA AC007255.8 promoter hypermethylation via upregulation of DNMT1 in Beas-2B cells, leading to downregulation of lncRNA AC007255.8, and ultimately the enhancement of cell proliferation and the inhibition of apoptosis. This research affords novel insights into the epigenetic mechanisms of lung cancer, and will stimulate further research into the involvement of aberrant DNA methylation of non-coding regions of the genome in the pathogenesis of lung cancer.

Fine particulate matter exposure induces DNA damage by downregulating Rad51 expression in human bronchial epithelial Beas-2B cells in vitro.

Although an accumulating body of evidence suggests that fine particulate matter (PM2.5) can cause lung injury and lung cancer, the underlying mechanisms are not yet clear. In this study, multiple endpoints associated with the cellular response to PM2.5 exposure, including the cell proliferation rate, cell apoptosis, malondialdehyde (MDA) content and DNA damage, were evaluated in human bronchial epithelial Beas-2B cells. The mRNA expression profile in PM2.5-treated cells was analyzed by transcriptome sequencing. The DNA repair gene Rad51 was then selected for further analysis. We found that the viability and growth of Beas-2B cells decreased while cell apoptosis increased in a dose-dependent manner after PM2.5 exposure. The comet assay showed that PM2.5 exposure induced evident DNA damage in PM2.5-treated cells. The MDA content in the treated cells was increased, indicating that PM2.5 exposure promoted lipid peroxidation. Furthermore, Rad51 expression was downregulated in PM2.5-treated cells, which may have contributed to the PM2.5-induced DNA damage in Beas-2B cells. Upregulation of Rad51 expression could rescue the negative impact of PM2.5 exposure in Beas-2B cells. Taken together, our research demonstrates that PM2.5 exposure induces DNA damage and impairs the DNA repair process by downregulating Rad51 expression in Beas-2B cells. This finding is expected to provide new insight into the genotoxicity of PM2.5 exposure.

The styrene purification performance of biotrickling filter with toluene-styrene acclimatization under acidic conditions.

The obvious disadvantages of biotrickling filters (BTFs) are the long start-up time and low removal efficiency (RE) when treating refractory hydrophobic volatile organic compounds (VOCs), which limits its industrial application. It is worthwhile to investigate how to reduce the start-up period of the BTF for treating hydrophobic VOCs. Here, we present the first study to evaluate the strategy of toluene induction combined with toluene-styrene synchronous acclimatization during start-up in a laboratory-scale BTF inoculated with activated sludge for styrene removal, as well as the effects of styrene inlet concentration (0.279 to 2.659 g·m-3), empty bed residence time (EBRT) (i.e., 136, 90, 68, 45, 34 sec), humidity (7.7% to 88.9%), and pH (i.e., 4, 3, 2.5, 2) on the performance of the BTF system. The experiments were carried out under acidic conditions (pH 4.5) to make fungi dominant in the BTF. The start-up period for styrene in the BTF was shortened to about 28 days. A maximum elimination capacity (ECmax) of 126 g·m-3·hr-1 with an RE of 80% was attained when styrene inlet loading rate (ILR) was below 180 g·m-3·hr-1. The highest styrene RE(s) [of BTF] that could be achieved were 95% and 93.4%, respectively, for humidity of 7.7% and at pH 2. A single dominant fungal strain was isolated and identified as Candida palmioleophila strain MA-M11 based on the 26S ribosomal RNA gene. Overall, the styrene induction with the toluene-styrene synchronous acclimatization could markedly reduce the start-up period and enhance the RE of styrene. The BTF dominated by fungi exhibited good performance under low pH and humidity and great potential in treating styrene with higher inlet concentrations. Implications: The application of the toluene induction combined with toluene-styrene synchronous acclimatization demonstrated to be a promising approach for the highly efficient removal of styrene. The toluene induction can accelerate biofilm formation, and the adaptability of microorganisms to styrene can be improved rapidly by the toluene-styrene synchronous acclimatization. The integrated application of two technologies can shorten the start-up period of biotrickling filters markedly and promote its industrial application.

Preparation and characterisation of activated carbon from waste tea by physical activation using steam.

In this study, the feasibility of preparing activated carbon from waste tea by physical activation using steam was investigated. The effects of activation temperature on yield and pore properties of the prepared activated carbon were studied. The yield decreased with increased activation temperature owing to the decomposition of cellulose and hemicellulose. The specific surface area and pore volume of the activated carbon were estimated using the Brunauer-Emmett-Teller method, Langmuir equation, and t-plot method. The specific surface area and micropore volume increased with increases in activation temperature, as additional volatile materials were released. The specific surface area significantly decreased at first but slightly increased with increasing activation time. The maximum specific surface area reached 995 m2/g at an activation temperature of 800 °C with a water flow rate of 0.075 g/min and a constant hold time of 0.5 hr. According to the nitrogen adsorption isotherms, micropores mainly developed when the activation temperature was below 800 °C, and both micropores and mesopores developed when it was above 800 °C. The results showed that activation temperature significantly affected micropore and mesopore volumes, as well as the specific surface area of the activated carbon. Overall, waste tea was found to be an attractive raw material for producing low-cost activated carbon. Implications: Every year, a large amount of waste tea is generated after extraction. The high carbon content of waste tea showed that it can be used as raw material to produce activated carbon. This study investigated the feasibility of preparing activated carbon from waste tea by physical activation using steam. Temperature and time were found to have clear effects on pore properties. Our proposed method and raw material are more environmentally friendly and involve low cost. Furthermore, this offers a potential solution to the problems of waste tea disposal and low-cost activated carbon production.

Extraction of phenol in wastewater with annular centrifugal contactors.

Solvent extraction is an effective way to treat and recover the phenolic compounds from the high content phenolic wastewater at present. The experimental study on treating the wastewater containing phenol has been carried out with QH-1extractant (the amine mixture) and annular centrifugal contactors. The distribution ratio of phenol was 108.6 for QH-1-phenol system. The mass-transfer process of phenol for the system was mainly controlled by diffusion. When the flow ratio (aqueous/organic) was changed from 1/1 to 4/1, the rotor speed was changed from 2500 to 4000 r/min, and the total flow of two phases was changed from 20 to 70 mL/min, the mass-transfer efficiency E of the single-stage centrifugal contactor was more than 95%. When the flow ratio was changed from 4.4/1 to 4.9/1, the rotor speed was 3000 r/min, and the total flow of two phases was changed from 43.0 to 47.0 mL/min, the extraction rate rho of the three-stage cascade was more than 99%. When 15% NaOH was used for stripping of phenol in QH-1, the stripping efficiency of the three-stage cascade was also more than 99% under the experimental conditions.

SHP-2 promotes the maturation of oligodendrocyte precursor cells through Akt and ERK1/2 signaling in vitro.

BACKGROUND: Oligodendrocyte precursor cells (OPCs) differentiate into oligodendrocytes (OLs), which are responsible for myelination. Myelin is essential for saltatory nerve conduction in the vertebrate nervous system. However, the molecular mechanisms of maturation and myelination by oligodendrocytes remain elusive. METHODS AND FINDINGS: In the present study, we showed that maturation of oligodendrocytes was attenuated by sodium orthovanadate (a comprehensive inhibitor of tyrosine phosphatases) and PTPi IV (a specific inhibitor of SHP-2). It is also found that SHP-2 was persistently expressed during maturation process of OPCs. Down-regulation of endogenous SHP-2 led to impairment of oligodendrocytes maturation and this effect was triiodo-L-thyronine (T3) dependent. Furthermore, over-expression of SHP-2 was shown to promote maturation of oligodendrocytes. Finally, it has been identified that SHP-2 was involved in activation of Akt and extracellular-regulated kinases 1 and 2 (ERK1/2) induced by T3 in oligodendrocytes. CONCLUSIONS: SHP-2 promotes oligodendrocytes maturation via Akt and ERK1/2 signaling in vitro.