Search

Hepatocellular carcinoma (HCC) is one of the most common cancers, and has an extremely poor prognosis. Our previous study confirmed that the microRNA miR-361-5p inhibited the proliferation, metastasis, invasiveness, and epithelial-to-mesenchymal transition (EMT) process of HCC by targeting the transcription factor Twist1. Long non-coding RNAs (lncRNAs) are key regulators of processes such as cell differentiation, inflammation, tumor formation, and immune escape. However, the underlying interactions between the lncRNA LINC00992, miR-361-5p, and Twist1 in HCC progression is still elusive. In the current study, the DIANA-lncBase database was used to identify regulatory genes upstream of miR-361-5p. Reverse transcription-quantitative PCR (RT-qPCR) was used to quantify the expression of the genes encoding LINC00992, miR-361-5p, and Twist1 in HCC cells. The cell counting kit-8 (CCK-8) was used to measure HCC cell proliferation and Transwell was used to measure HCC cell migration and invasion. The dual-luciferase reporter assay and RNA pull-down assay were performed to examine the interaction between LINC00992 and miR-361-5p. Western blotting was used to detect the levels of Twist1 protein. The result confirmed that, among three lncRNAs tested, miR-361-5p was the one most significantly affected by LINC00992. RT-qPCR revealed that LINC00992 was highly expressed in HCC tissues and cells. The follow-up results showed that the expression of LINC00992 and miR-361-5p in HCC tissues were closely correlated with the rate of metastasis or recurrence of the HCC patients. Our result showed that the expression of miR-361-5p was lower in the LINC00992 (+) group than in the LINC00992 (-) group. CCK-8 and Transwell showed that LINC00992 promoted HCC cell proliferation, migration, and invasion, whereas dual-luciferase reporter assay and RNA pull-down assay showed that LINC00992 combined with miR-361-5p to act as a miRNA decoy in HCC. RT-qPCR and Western blotting confirmed that LINC00992 upregulated the expression of the Twist1 gene in HCC cells by downregulating expression of miR-361-5p. CCK-8 and Transwell assays confirmed that LINC00992 promoted the proliferation, metastasis, and invasiveness of HCC cells by downregulating miR-361-5p levels and consequently upregulating Twist1 expression, implying that these three elements may be promising targets for HCC therapy.

Arsenic is either notorious toxicant or miracle cure for acute promyelocytic leukemia and several other diseases. It interacts with mitochondria directly or indirectly, by interacting with mitochondrial enzymes, such as respiratory chain complexes and tricarboxylic acid cycle proteins, or affecting mitochondrial homeostasis via ROS or mitochondrial outer membrane permeabilization. Given the ubiquitous presence of mitochondria and indispensable role in cellular metabolism, arsenical-mitochondrial interactions may manifest clinical importance by revealing mechanism of disease curation, preventing severe side effects, and foreseeing potential health issues. Here, we described the interaction between isolated mitochondria and arsenicals.

At a time when game-based learning has become a research hotspot, this study focused on the competition mechanism in gamified learning, aiming to explore the impact of different competition modes on students’ vocabulary learning effect and learning motivation. A group of 79 sixth grade students from China were randomly assigned to a non-competitive class, an individual competition class, and an inter-group competition class. The experiment was conducted in an English vocabulary course, and the game competition was carried out using the Quizlet Live game platform. The results indicated that: (1) the vocabulary learning effect and motivation of students in the competitive classes (individual competition and inter-group competition) were better than those in the non-competitive class; (2) the learning effect of students in the inter-group competitive class outperformed that of the individual competitive class, but there was no significant difference in learning motivation. Through the qualitative analysis of the students’ interviews, it was found that the results of inter-group competition may be related to the student’s perception of learning and emotional support. The findings of this study can provide relevant support for the subsequent game-based learning design.

Although increasing evidence has confirmed that the apoptosis of renal tubular epithelial cells (RTECs) is a crucial contributor to the onset and development of septic acute kidney injury (AKI), the pathological mechanism by which RTEC apoptosis is upregulated during septic AKI is not entirely clear. In this study, a rat model of septic AKI was induced by a cecal ligation puncture procedure or lipopolysaccharide (LPS) injection. Four differentially expressed long noncoding RNAs (DE-Lncs) in the rat model of septic AKI were determined using RNA-sequencing and verified by qRT-PCR. Among the four DE-Lncs, the expression level of lncRNA NONRATG019935.2 (9935) exhibited the most significant reduction in both septic AKI rats and LPS-treated NRK-52E cells (a rat RTEC line). The overexpression of 9935 suppressed cell apoptosis and p53 protein level in LPS-treated NRK-52E cells, and retarded septic AKI development in the rat model of septic AKI. Mechanistically, 9935 decreased the human antigen R (HuR)-mediated Tp53 mRNA stability by limiting the combination of HuR and the 3′UTR region of Tp53 mRNA in RTECs. The overexpression of HuR abrogated the inhibitory effect of pcDNA-9935 on the LPS-induced apoptosis of NRK-52E and rat primary RTECs. In conclusion, 9935 exerts its role in septic AKI by suppressing the p53-mediated apoptosis of RTECs, and this essential role of 9935 relies on its destructive effect on HuR-mediated Tp53 mRNA stability.

Background Kashin-Beck disease (KBD) is an endemic osteoarthropathy, and its pathogenesis is still not entirely clear. Pathologically, many KBD changes are similar to those of osteoarthritis (OA). Therefore, this study aimed to identify changes in the levels of potential urinary biomarkers for OA, including C-telopeptide of type II collagen (uCTX-II), type II collagen cleavage neoepitope (uC2C), pyridinoline (uPYD), and uHelix-II, among adults with KBD. Methods Urinary samples of 83 external control (EC) subjects, 91 KBD patients, and 86 internal control (IC) subjects were tested by ELISA after the subjects completed a questionnaire and X-ray examination. Results The medians of the four markers in the KBD group were higher than those in the EC group and those in the IC group. The medians in the grade II KBD group were higher than those in the grade I group but were not statistically significant (P = 0.301, P = 0.408, P = 0.204, and P = 0.898 for uCTX-II, uC2C, uPYD, and uHelix-II, respectively). The area under the curve (AUC) of uCTX-II (0.775) was higher than that of the others (0.672, 0.639, and 0.628 for uC2C, uPYD, and uHelix-II, respectively). Conclusion The levels of uCTX-II, uC2C, uPYD, and uHelix-II were elevated in adults with KBD and showed an increasing trend as the severity of KBD increased. The prediction accuracy of uCTX-II was more useful than that of the others for assisting in the diagnosis of KBD.

To investigate the effect of Bmi-1 gene silencing on the proliferation of K562/ADM cells in vitro and in vivo and to explore its possible molecular mechanism.The small interference RNA (siRNA) sequences of Bmi-1 were transfected into K562/ADM cells for decreasing the expression of Bmi-1. The effect of Bmi-1 silencing on the proliferation of K562/ADM cells in vitro and in vivo was detected by using MTT method, cell colony-forming test and tumoriganicity of nude mice; the expression of Bmi-1, PTEN and PAKT proteins was detected by Wertern blot. The immunohistochemistry assay was used to analyze the expression of Bmi-1 and Ki-67.The Bmi-1 silencing could significantly inhibit the proliferation activity of K562/ADM cells, the cell colony-forming ability and tumorigenicity were reduced. LY294002 decreased p-AKT expression, cell colony-forming ability and tumorigenicity. Bpv reduced the PTEN expression but increased p-AKT expression and restored the colony-forming ability and tumorigenesis of K562/ADM-S1-Bpv cells. Bmi-1-siRNA dramatically suppressed the Bmi-1 and Ki-67 protein levels in xenograft tumor tissue.Bmi-1 can mediate the proliferation of K562/ADM cell, the PTEN/p-AKT might be involved in this pathway.沉默Bmi-1表达对K562/ADM细胞体内外增殖能力的影响.观察沉默Bmi-1表达对慢性髓系白血病阿霉素耐药细胞株-K562/ADM细胞增殖的影响并初步探讨其分子机制.将Bmi-1小干扰RNA（siRNA）序列转染到K562/ADM细胞中降低其Bmi-1的表达；采用MTT法、软琼脂集落形成实验、裸鼠成瘤实验检测沉默Bmi-1表达对K562/ADM细胞体内外增殖能力的影响；应用Western blot检测Bmi-1、PTEN、p-AKT等蛋白表达；免疫组织化学实验分析Bmi-1和Ki-67的表达情况.Bmi-1基因的沉默能够抑制K562/ADM细胞的增殖活性、集落形成及裸鼠成瘤能力；Bmi-1基因沉默后，干扰组PTEN表达明显升高，而p-AKT活性明显下降；p-AKT抑制剂-LY294002处理K562/ADM细胞后，p-AKT表达降低，集落形成及裸鼠成瘤能力相比K562/ADM细胞降低；PTEN抑制剂-Bpv处理K562/ADM-S1细胞后，PTEN的表达降低，而p-AKT表达、集落形成及裸鼠成瘤能力得以重塑； Bmi-1基因沉默使得肿瘤组织中Bmi-1与Ki-67表达均下降.Bmi-1基因有可能参与了对K562/ADM的体内外增殖能力的调控，PTEN/pAKT信号通路可能涉及其中.

Based on the potential therapeutic value in targeting mitochondria and the fluorophore tracing ability, a fluorescent mitochondria-targeted organic arsenical PDT-PAO-F16 was fabricated, which not only visualized the cellular distribution, but also exerted anti-cancer activity in vitro and in vivo via targeting pyruvate dehydrogenase complex (PDHC) and respiratory chain complexes in mitochondria. In details, PDT-PAO-F16 mainly accumulated into mitochondria within hours and suppressed the activity of PDHC resulting in the inhibition of ATP synthesis and thermogenesis disorder. Moreover, the suppression of respiratory chain complex I and IV accelerated the mitochondrial dysfunction leading to caspase family-dependent apoptosis. In vivo, the acute promyelocytic leukemia was greatly alleviated in the PDT-PAO-F16 treated group in APL mice model. Our results demonstrated the organic arsenical precursor with fluorescence imaging and target-anticancer efficacy is a promising anticancer drug.

Water quality is a critical factor in the treatment of Microcystis aeruginosa–contaminated water sources. In this paper, we report on a pressure pretreatment method that is safer than the t...

A novel reaction-based turn-on fluorescent BODIPY probe for the detection of biothiols was designed and synthesized. The sensitivity and selectivity of the probe were greatly enhanced by introduction of dual reactive groups, which simultaneously acted as fluorescence quenching units. The probe had fluorescence enhancement of up to 106-fold, 56-fold and 77-fold in the presence of Hcy, Cys and GSH, respectively. This probe had stable fluorescence emission within physiological pH range and exhibited low cytotoxicity. The background of the probe was quite low and medium wash was not required in cell imaging. This probe could rapidly image intracellular biothiols in ca. 10 min, and selectively accumulated in mitochondria.

In order to clarify the mitochondrial toxicity mechanism of the organic arsenical MOPIMP (2-methoxy-4-(((4-(oxoarsanyl) phenyl) imino) methyl) phenol), research was carried out at the sub-cell level based on the previous finding that the compound MOPIMP can damage the mitochondria by triggering a burst of ROS. After investigating its influence on isolated mitochondria in vitro, it was demonstrated that a high dose of MOPIMP with short-term exposure can induce mitochondrial swelling, decrease the membrane potential, enhance the permeability of H+ and K+, and induce membrane lipid peroxidation, indicating that it can result in an MPT process in a ROS-mediated and Ca2+-independent manner. Additionally, MPT was also aggravated as a result of impairment of the membrane integrity and membrane fluidity. In addition, short-term incubation between mitochondria and compound MOPIMP promoted the inhibition of respiratory chain complexes I, II, III and IV, as well as damage to the respiration process, which supported the previous finding about the burst of ROS. On the other hand, after long-term exposure by the organic arsenical MOPIMP, mitochondrial metabolic dysfunction was triggered, which was in accordance with perturbation of the respiratory chain complexes as well as the respiration process. This work systematically sheds light on the mitochondrial toxicity mechanism of the organic arsenical MOPIMP, including induction of the MPT process and inhibition of respiratory metabolism, which provides a potential target for organic arsenicals as anti-tumor drugs.

Considering the vital role of cellular redox state, more and more researches focus on the design of drugs targeting thioredoxin reductase (TrxR), an important enzyme in maintaining the balance of cellular redox. Here two organic arsenicals, 2-(((4-(1,3,2-dithiarsinan-2-yl) phenyl) imino) methyl) phenol (PIM-PAO-PDT) and N-(4-(1,3,2-dithiarsinan-2-yl) phenyl)-2-hydroxybenzamide (PAM-PAO-PDT), bearing the S-As-S chemical scaffold and different linking groups have been synthesized, and both of them show the better inhibitory activity and selectivity towards HL-60 cells. Importantly, it is illustrated that they can target TrxR selectively and inhibit its activity via the disturbance for Cys83 and Cys88 located in conserved active sites. Afterwards, the cells suffer from the burst of ROS, consumption of antioxidants and high sensitivity for oxidants, which further damage the mitochondria leading to dysfunction including the collapse of membrane potential, ATP level decline, mitochondrial membrane swelling, MPTP opening, Ca2+ and cytochrome c release. Then the mitochondria-dependent apoptosis is triggered by PIM-PAO-PDT and PAM-PAO-PDT, which can also be deterred in the presence of NAC, DTT or LA. Although the organic arsenicals can suppress TrxR activity, the following oxidative stress and mitochondrial dysfunction are the main causes for apoptosis.

While Indium's toxicity to organs is realized, its effects on mitochondria are still under investigation. Mitochondrial permeability transition (MPT) is widely accepted in mitochondrial dysfunction approaches and its importance in metal-induced mitochondrial degradation has been proposed. Since mitochondria are respiratory organelles, their interaction with free In3+ is analyzed to access structural and functional changes. Spectral methods and multimode plate reader was used to detect mitochondrial swelling, membrane potential, membrane fluidity, and inner membrane permeability. Flow cytometry was employed to detect mitochondrial reactive oxygen species (ROS) generation and transmission electron microscopy to image mitochondria. And oxygen electrode was used to measure respiratory rate, microcalorimetry to monitor long-term real-time mitochondrial metabolism. In3+ at a concentration up to 1mM induces mitochondrial swelling, membrane depolarization and inhibits the protons transportation. In3+-induced mitochondrial swelling and membrane depolarization is protected by MPT inhibitors and -SH protectors, but the influence on protons transportation is not protected. In addition, In3+ is able to accelerate the ROS production and inhibit the electron transition and respiratory chain while it stimulates long-term metabolism. Our findings show that In3+ induces MPT by inhibiting the proton channels located in the inner mitochondrial membrane and by stimulating mitochondrial oxidative stress.

Purpose Due to the rise in urbanization, demand for easily prepared foods such as pastries and noodles has risen. But the high price of wheat in the global market puts financial stress on low-income people, especially on those living in tropical regions, where wheat does not thrive well. They depend solely on imported wheat, which is expensive due to importation cost, or seek other relatively less-nutritious cereals. Therefore the purpose of this paper is to investigate the possibility of supplementing wheat flour with flour from relatively cheap and easy-to-produce root tuber, such as cassava, potato and sweet potato. Design/methodology/approach Strong-, medium- and weak-gluten wheat flours were supplemented with flour from cassava, potato and sweet potato at 10, 20 and 30 percent. Strong gluten composites were used to make bread, whereas medium and weak gluten composites were used for cookie and noodle production, respectively. Protein, ash, fat, crude fiber, moisture, carbohydrate, gluten, zeleny and energy contents of each composite were tested. Findings The nutritional and sensory quality of bread, cookies and noodles made from wheat flour supplemented with root tuber flour at 10, 20 and 30 percent was assessed. Results revealed that mixing wheat flour and root tuber flour has important effects on the moisture, protein, carbohydrate, fat, ash, gluten, zeleny sedimentation value and crude fiber content of the resulting mixture. Moisture and carbohydrate increased while protein and fat significantly (p Originality/value This work has successfully confirmed that wheat flour could be supplemented up to 20 percent with root tuber flour without compromising the nutritional and sensory quality of products. It has also demonstrated that different products require different root tuber flour substitution for optimum results. Potato at 10 percent substitution was found to be best for bread production. Cassava and sweet potato at 10 percent substitution were also best for cookies and noodles, respectively. With respect to protein content only, sweet potato substitution is better than cassava and potato.

A simple acylhydrazone derivative 4-chloro-N′-(pyridin-2-ylmethylene) benzo- hydrazide (CPBH) has been designed to be a fluorescence probe for Al3+. CPBH displays a highly sensitive and selective fluorescence enhancement with Al3+ among various metal ions, due to a reduced intramolecular charge transfer and chelation enhanced fluorescence mechanism. The limit of dection for Al3+ is 0.2 μM (5.4 ppb), and the linear range is from 2 to 15 μM (50–400 ppb, c(CPBH) = 20 μM) in the low concentration while another linear range is from 20 to 80 μM (540–2200 ppb, c(CPBH) = 100 μM). The CPBH and Al3+ form a 2:1 coordination complex according to the ESI-MS, Job plots and spectroscopy data. The binding equilibrium constant K is about 4.69 × 104 M−1 and 3.68 × 104 M−1 based on the data from absorption and emission spectra, respectively. To conclude, CPBH can be used as a sensitive and selective fluorescent probe for Al3+.

Silver, once regarded as a safe noble metal for humans, has been widely used in industrial and commercial products, especially in nanometer biomaterials. It is now well known that Ag+ is biologically active and is able to interact with the cell membrane, proteins and DNA. However, very little is understood about the potential impacts of Ag+ at the sub-cellular level. Our work investigated the potential toxicity of Ag+ on mitochondria isolated from rat livers by examining the mitochondrial morphology, respiration, swelling, membrane fluidity and reactive oxygen species (ROS) generation. We observed that Ag+ significantly affects the mitochondrial structure and function, including mitochondrial swelling, collapse of the transmembrane potential, change of permeability and fluidity, decline of the respiratory rate, and acceleration of ROS, indicating that Ag+ should be seriously regarded as a potentially hazardous substance. Moreover, we conclude that Ag+ injures the mitochondrial structure and function by a nonspecific approach, in which the interaction is unregulated by inherent parts such as the mitochondria permeability transition pore (MPTP). These results help us learn more about the toxicity of Ag+ at the subcellular (mitochondrial) level and influence future biological and medical applications of Ag-based materials.

To investigate the effect of Bmi-1 gene silence on the proliferation ability of K562 cells in vitro and in vivo, and to explore the relation of molecular mechanism between proliferation ability of K562 cells in vitro and in vivo with PTEN/pAKT signaling pathway.The Bmi-1 small interference RNA (siRNA) sequences were transfected into K562 cells for decreasing Bmi-1 expression. The effect of Bmi-1 siRNA on the proliferation of K562 cells in vitro and in vivo was detected by MTT method and colony-forming test, the effect of Bmi-1 siRNA on the tumorogenicity of K562 cells was observed by subcutaneous inoculation of K562 cells, LY294002 and Bpv treated K562 cells in nude mice, the expression of Bmi-1, PTEN and pAKT proteins were detected by Western blot.The Bmi-1 siRNA could inhibit the proliferation activity, colony-forming and tumor-forming abilities of K562 cells. After the silence of Bmi-1 gene, the PTEN expression in Bmi-1 gene-silenced group was significantly enhanced. While the pAKT expression in Bmi-1 gene-silenced group was significantly reduced; after the K562 cells were treated with LY294002 (an inhibitor of pAKT), the pAKT expression colony-forming and tumor forming abilities were reduced in comparison with untreated K562 cells; after the K562-S1 cells were treated with Bpv (an inhibitor of PTEN), the PTEN expression decreased, while the pAKT expression, colony forming and tumor-forming abilities were restored.The Bmi-1 gene possibly involves in regulation of K562 proliferation in vivo and in vitro, the effect of PTEN/pAKT signaling pathway maybe one of molecular mechanisms mediating this regulation.Bmi-1-siRNA通过PTEN/pAKT通路调控K562细胞体内外的增殖能力.观察Bmi-1基因沉默对白血病K562细胞体内外增殖能力的影响并初步探究二者之间的分子机制是否与PTEN/pAKT通路有关.将Bmi-1小干扰RNA（siRNA）序列转染到K562细胞中降低其Bmi-1的表达；应用MTT比色法和软琼脂集落形成实验检测Bmi-1- siRNA对K562细胞体外增殖的影响；裸鼠皮下接种各组细胞，观察Bmi-1- siRNA对K562细胞在裸鼠体内的致瘤能力的影响；应用Western blot检测Bmi-1、PTEN、p-AKT等蛋白的表达.Bmi-1-siRNA有效沉默了Bmi-1基因mRNA和蛋白的表达；沉默Bmi-1基因的表达能够抑制K562细胞的增殖活性、集落形成及裸鼠成瘤能力；Bmi-1基因沉默后，干扰组PTEN表达明显升高，而p-AKT活性明显下降；p-AKT抑制剂LY294002处理K562细胞后，p-AKT表达降低，集落形成及裸鼠成瘤能力相比未处理K562细胞降低；PTEN抑制剂Bpv处理K562-S1细胞后，PTEN的表达降低，而p-AKT、集落形成及裸鼠成瘤能力得以重塑.Bmi-1基因有可能参与了对白血病细胞K562的体内外增殖能力的调控，PTEN/pAKT信号通路可能是介导这一调控过程的分子机制之一.

Considering the vital role of mitochondria in the anti-cancer mechanism of organic arsenical, the mitochondria-targeted precursor PDT-PAO-TPP was designed and synthesized. PDT-PAO-TPP, as a delocalization lipophilic cation (DLCs) which mainly accumulated in mitochondria, contributed to improve anti-cancer efficacy and selectivity towards NB4 cells. In detail, PDT-PAO-TPP inhibited the activity of PDHC resulting in the suppression of ATP synthesis and thermogenesis disorder. Additionally, the inhibition of respiratory chain complex I and IV by short-time incubation of PDT-PAO-TPP also accelerated the respiration dysfunction and continuous generation of ROS. These results led to the release of cytochrome c and activation of caspase family-dependent apoptosis. Different from the mechanism of PDT-PAO in HL-60 cells, it mainly induced the mitochondrial metabolic disturbance resulting in the intrinsic apoptosis via inhibiting the activity of PDHC in NB4 cells, which also implied that the efficacy exertion of organic arsenical was a complex process involved in many aspects of cellular function. This study systematically clarifies the anti-cancer mechanism of mitochondria-targeted organic arsenical PDT-PAO-TPP and confirms the new target PDHC of organic arsenicals, which further supports the organic arsenical as a promising anticancer drug.

Based on the potential therapeutic value in targeting metabolism for the treatment of cancer, an organic arsenical PDT-BIPA was fabricated, which exerted selective anti-cancer activity in vitro and in vivo via targeting lactate dehydrogenase A (LDHA) to remodel the metabolic pathway. In details, the precursor PDT-BIPA directly inhibited the function of LDHA and converted the glycolysis to oxidative phosphorylation causing ROS burst and mitochondrial dysfunction. PDT-BIPA also altered several gene expression, such as HIF-1&alpha, and C-myc, to support the metabolic remodeling. All these changes lead to caspase family-dependent cell apoptosis in vivo and in vitro without obvious side effect. Our results provided this organic arsenical precursor as a promising anticancer candidate and suggested metabolism as a target for cancer therapies.

Battery switch station (BSS) can resolve the conflict between life and charging time of batteries of electric vehicles by offering quick replacement services though pre-charging with small power. This paper proposed an energy management model for BSS in two settlement electricity markets. The present program focused on how to satisfy demands of electric vehicles with lowest cost in electricity markets, which are the key issue of lowering operating costs of BSS. The program adopted the mean-variance theory to control financial risks of uncertainties of prices, and simulation results showed the effectiveness of the proposed program

Arsenic trioxide has shown the excellent therapeutic efficiency for acute promyelocytic leukemia. Nowadays, more and more research focuses on the design of the arsenic drugs, especially organic arsenicals, and on the mechanism of the inducing cell death. Here we have synthesized some organic arsenicals with Schiff base structure, which showed a better antitumor activity for three different kinds of cancer cell lines, namely HL-60, SGC 7901 and MCF-7. Compound 2a (2-(((4-(oxoarsanyl)phenyl)imino)methyl)phenol) and 2b (2-methoxy-4-(((4-(oxoarsanyl)phenyl)imino)methyl)phenol) were chosen for further mechanism study due to their best inhibitory activities for HL-60 cells, of which the half inhibitory concentration (IC50) were 0.77 μM and 0.51 μM, respectively. It was illustrated that 2a or 2b primarily induced the elevation of reactive oxygen species, decrease of glutathione level, collapse of mitochondrial membrane potential, release of cytochrome c, activation of Caspase-3 and apoptosis, whereas all of the phenomena can be eliminated by the addition of antioxidants. Therefore, we concluded that compound 2a and 2b can induce the oxidative stress-mediated intrinsic apoptosis in HL-60 cells. Both the simplicity of structure with Schiff base group and the better anticancer efficiency demonstrate that organic arsenicals are worthy of further exploration as a class of potent antitumor drugs.

This paper reviews the harmonic current detection algorithm of APF&SVG. And the new different research of each detection method is introduced. The advantage and disadvantage of each methods is also analyzed. It has provided some references to the electric current detection algorithm choice for the design of the APF and SVG.

This paper analyzes the construction and control principle of Thyristor Switched Capacitor(TSC) and Active Power Filter(APF) integrated device. An harmonics detection method based on the instantaneous reactive power theory is also discussed. This method is effective to apply to TSC&APF integrated device and can get better result to eliminate the harmonics and compensate reactive power. A new integrated device which consists of TSC and APF is developed with this method. The application in the automobile industry shows that this device is correct and effective. It is a favorable model of improving the power quality and save the energy.

A study on the wear of Quick-point grinding wheel was carried on. The wheel wear was found having great influence on grinding performance and grinding quality. After analyzed the wear process and mechanism in Quick-point grinding, it was found the wear rate was directly related to some factors such as wheel width, workpiece speed, feed rate and Quick-point grinding angle, and it was indirectly affected by wheel speed and cutting depth. By means of some wear criteria, the wheel wear was able to be predicted. Furthermore, a wear model in wheel’s accurate area has been built up.

Pressure enhanced coagulation and sedimentation technique is an effective way for blue algae treatment. It is not clear whether Cyanobacteria balloon rupture will cause Cyanobacteria cells rupture, resulting in high intracellular concentrations of microcystin LR leak into the water, affecting drinking water safety. Therefore, in this study experimental comparative study of pressure and pre-oxidation of water containing Cyanobacteria was carried out to examine the microcystin LR concentration changes and Cyanobacteria removal efficiency. The results showed that microcystin concentration increase was not significant by the pre-treatment with Cyanobacteria water pressure, while the pre-oxidation process caused a significant increase in the concentration of microcystin. After 0.5-0.8 MPa pressure coagulation and sedimentation, removal of Cyanobacteria basically was over 90%, up to 93.5%, while the removal rate by pre-oxidation was low and unstable. Effluent turbidity is also significantly better in the pre-pressure method than the pre-oxidation. The results indicated that pressure enhanced coagulation is a safe and reliable method for Cyanobacteria removal.

The aim of the study was to explore whether the pre-pressure and coagulation sedimentation process would result in algal cell disruption, leading to increased dissolved organic carbon (DOC) in water, based on which, the pressure application mode would be optimized and safe and efficient pre-pressure algae removal process would be obtained. The changes in DOC during the process of pre-pressure and preoxidation treatment, the distribution of molecular weight in water as well as the removal efficiency of algae, turbidity and DOC after coagulation and sedimentation were investigated. The results showed that the DOC in water did not increase but decreased, and the molecular weight decreased after treated with 0.5-0.8 MPa pressure. While KMnO4 and NaClO pre-oxidation both increased the DOC, in the meanwhile, the distribution of molecular weight showed no obvious change. After the pre-pressure coagulation and sedimentation process, the removal rate of algae was 96.23% and that of DOC was 29. 11%, which was by 10% - 30% higher than the rate of pre-oxidation coagulation and sedimentation process.

An acidophilic iron-sulfur oxidizing bacterium LY01 was isolated from acid mine drainage of coal in Guizhou Province, China. Strain LY01 was identified as Acidithiobacillusferrooxidans by morphological and physiological characteristics, and phylogenetic analysis of its 16S rRNA gene sequence. Strain LY01 was able to grow using ferrous ion (Fe2+), elemental sulfur (S0) and pyrite as sole energy source, respectively, but significant differences in oxidation efficiency and bacterial growth were observed when different energy source was used. When strain LY01 was cultured in 9K medium with 44.2 g x L(-1) FeSO4.7H2O as the substrate, the oxidation efficiency of Fe2+ was 100% in 30 h and the cell number of strain LY01 reached to 4.2 x 10(7) cell x mL(-1). When LY01 was cultured in 9K medium with 10 g x L(-1) S0 as the substrate, 6.7% S0 oxidation efficiency, 2001 mg x L(-1) SO4(2-) concentration and 8.9 x 10(7) cell x mL(-1) cell number were observed in 21 d respectively. When LY01 was cultured with 30 g x L(-1) pyrite as the substrate, the oxidation efficiency of pyrite, SO4(2-) concentration and cell number reached 10%, 4443 mg x L(-1) and 3.4 x 10(8) cell x mL(-1) respectively in 20 d. The effects of different heavy metals (Ni2+, Pb2+) on oxidation activity of strain LY01 cultured with pyrite were investigated. Results showed that the oxidation activity of strain LY01 was inhibited to a certain extent with the addition of Ni2+ at 10-100 mg x L(-1) to the medium, but the addition of 10-100 mg x L(-1) Pb2+ had no effect on LY01 activity.