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Cubic phase, monodispersed size and uniform shape Cu2GeTe3 nanocrystals exhibiting excellent optoelectronic properties have been for the first time synthesized by a facile colloidal method.

BACKGROUND It has been reported that the polyadenylate-binding protein-interacting protein 1 (PAIP1) pathway is closely connected with the progression of some malignant tumors. Here we examined the potential functional mechanism of PAIP1 in tongue squamous cell carcinoma (TSCC). METHODS PAIP1 was knocked down in TSCC cell lines and proliferation and apoptosis in vitro analyzed. The molecular features of TSCC were determined using quantitative proteome and succinylome analyses. The results were confirmed in the mouse model. RESULTS PAIP1 promoted cell proliferation and inhibited apoptosis. Its knockdown decreased Ki67 and Pcna expressions and increased Bax/Bcl2 index and Caspase-3 expression. Bioinformatics analysis for proteomics revealed that PAIP1 knockdown correlated with the changes in differential protein expression. CONCLUSIONS Upregulation of PAIP1 induces cell proliferation and inhibits apoptosis in TSCC; PAIP1 might be a diagnostic biomarker and a significant drug target.

This article was designed by using a network pharmacological approach to reveal the therapeutic targets and molecular mechanisms of oxyresveratrol (Oxyres) treating colorectal cancer (CRC). Furthermore, several bioinformatic findings would be validated. Pathogenetic targets of CRC and pharmacological targets of Oxyres were identified by web-available databases. All identifiable biotargets were collected for functional enrichment analyses to reveal the biological processes and signaling pathways of Oxyres treating CRC. In addition, human CRC, non-CRC samples, and cell line study were used to validate the predictive biotargets of Oxyres treating CRC. In network pharmacological analyses, top therapeutic targets of mitogen-activated protein kinase 1 (MAPK1), insulin growth factor 1 (IGF1), hematopoietic prostaglandin D synthase (HPGDS), GTPase HRas (HRAS), and cytochrome P450 2C9 (CYP2C9) in Oxyres treating CRC were identified, respectively. As shown in functional analysis, biological processes of Oxyres treating CRC were mainly involved in modulating cell communication, signal transduction, apoptosis, cell motility, cell proliferation, and lipid metabolism. Furthermore, top 10 signaling pathways of Oxyres treating CRC were identified, respectively. In human study, CRC samples resulted in increased neoplastic expressions of Ki-67, MAPK1, IGF1, characterized with clinical imaging inspection, pathological diagnosis, and altered blood lipids in these CRC cases. In cell culture study, Oxyres-dosed CRC cells exhibited reduced cell proliferation, promoted cellular apoptosis. Furthermore, significantly decreased proteins of intracellular Ki-67, MAPK1, and IGF1 were observed in Oxyres-dosed cells when compared to those in controls. Collectively, anti-CRC pharmacological activity of Oxyres may be mainly associated with induction of apoptosis and suppression of cell proliferation as revealed in bioinformatic findings. In addition, all core biotargets and molecular mechanisms of Oxyres treating CRC are unveiled respectively. Interestingly, the identifiable MAPK1, IGF1 biotargets may be potential molecules for treating and screening CRC.

Enhanced biological phosphorus removal (EBPR) technology has been widely considered as a key strategy in preventing eutrophication and recognized as the advancing front of research in wastewater treatment. The key to keep its high efficiency in biological phosphorus removal is to optimize the operation and management of the system. Previous research in this field has undoubtedly improved understanding of the factors hindered overall efficiency of EBPR. However, it is obvious that much remains to be learnt. This paper attempts to review the fundamental understanding in factors inhibiting the stability and reliability of the EBPR systems in the state-of-the-art research. In view of modeling the EBPR systems, an appropriate extension of the current mechanistic models with these inhibitory factors is recommended in order to better simulate and predict the behavior of full-scale and lab-scale EBPR plants. From the perspectives of the further mechanistic and multi-factors study, the direction of denitrifying dephosphatation and granules/biofilms are also discussed. This comprehensive overview will not only help us to understand the overall mechanism of the EBPR process, but also benefit the researchers and engineers to consider all the possible factors affecting the process in the urban sewage treatment plants.

Influence of Cr(VI) on P removal in enhanced biological phosphorus removal (EBPR) system was investigated with respect to the composition of poly-phosphate-accumulating organisms (PAOs) and glycogen accumulating organisms (GAOs), the transformation of poly-β-hydroxyalkanoates (PHA) and glycogen, enzymes’ activities, and the intracellular Cr. Whether EBPR system could revive after Cr(VI) shock was also explored. Results showed P removal performance was completely inhibited by Cr(VI) with the concentration more than 5 mg L−1. PAOs were more sensitive to Cr(VI) than GAOs and the other bacteria were. PHA consumption, glycogen synthesis and adenylate kinase’s activity had been inhibited by 5 mg L−1 Cr(VI). Both adenylate kinase’s activity and P removal efficiency were negatively correlated with the intracellular Cr. Recovery experiments revealed that P removal performance with 5 mg L−1 Cr(VI) shock could revive after a 2-day recovery treatment, while systems with high level Cr(VI) (20 and 60 mg L−1) shock could not.

The roles of the G-protein-linked thrombin receptor and platelet glycoprotein Ib (GPIb) as alpha-thrombin-binding sites on platelets remain controversial. alpha-Thrombin has been proposed to bind to both GPIb and the hirudin-like domain of the G-protein-linked receptor (from which it cleaves the NH2-terminal extracellular domain to release a 41-mer peptide (TR-(1-41), where TR is alpha-thrombin receptor)) to initiate platelet activation. Using affinity-purified rabbit anti-human TR-(1-41) IgG and immunoblotting, we demonstrated TR-(1-41) release from platelets suspended in Tyrode's buffer containing 2 mM CaCl2 and incubated with >/=0.5 nM alpha-thrombin for 10-60 s at 37 degrees C. As quantified by enzyme-linked immunosorbent assay, 0.32-0.59 nM TR-(1-41) was released from washed platelets (5 x 10(11) platelets/liter) after their incubation with 10 nM alpha-thrombin for 10 s. Parallel binding of alpha-thrombin to and activation of the platelets were confirmed by flow cytometry. A monoclonal antibody against the hirudin-like domain of the G-protein-linked receptor abrogated alpha-thrombin binding to platelets, cleavage of TR-(1-41), and platelet activation by

The inhibition of free ammonia (FA) to the granule-based enhanced biological phosphorus removal (EBPR) system and the recoverability from macro- to micro-scale were investigated in this study. FA was found to seriously deteriorate the EBPR performance and sludge characteristic (settleability and morphology). The FA inhibitory threshold of 17.76 mg N L −1 was established. Acclimation phenomenon took place when poly-phosphate accumulating organisms (PAOs) were exposed for long time to constant FA concentration (8.88 mg N L −1 ). The repressed polysaccharides excretion could lead to breaking the stability and integrity of the granules. Therefore, the reduced particle size and granule disintegration were observed. The molecular analysis revealed that FA had a significant influence on the microbial communities and FA inhibition may provide a competitive advantage to glycogen accumulating organisms (GAOs) over PAOs. Interestingly, the community composition was found irreversible by recovery (Dice coefficients, 36.3%), although good EBPR performance was re-achieved.

An optimal operating condition for ammonia removal at low temperature, based on fully coupled activated sludge model (FCASM), was determined in a full-scale oxidation ditch process wastewater treatment plant (WWTP). The FCASM-based mechanisms model was calibrated and validated with the data measured on site. Several important kinetic parameters of the modified model were tested through respirometry experiment. Validated model was used to evaluate the relationship between ammonia removal and operating parameters, such as temperature ( T ), dissolved oxygen (DO), solid retention time (SRT) and hydraulic retention time of oxidation ditch (HRT). The simulated results showed that low temperature have a negative effect on the ammonia removal. Through orthogonal simulation tests of the last three factors and combination with the analysis of variance, the optimal operating mode acquired of DO, SRT, HRT for the WWTP at low temperature were 3.5 mg L −1 , 15 d and 14 h, respectively.

This study investigated the long-term effect of nitrite on the granule-based enhanced biological phosphorus removal (EBPR) system and the reversibility from macro- to micro-scale. Nitrite was found to seriously deteriorate the EBPR performance and result in severe sludge bulking. The inhibited polysaccharides excretion could lead to breaking the stability and integrity of the granules. Therefore, the reduced particle size and granule disintegration were observed. In this study, granules with lower ratio of proteins to polysaccharides (1.76) had better structure and function than the higher (3.84). Experimental results demonstrated that the microbial community structure was largely changed due to the presence of nitrite. In comparison, glycogen accumulating organisms (GAOs) had stronger resistibility and higher recovery rate than poly-phosphate accumulating organisms (PAOs). Interestingly, the community composition was unable to recover (Dice coefficients, 33.0%), although good EBPR performance was achieved only by propagating other types of PAOs.

A symbiotic ecosystem between Tubificidae and microorganisms was established at a full-scale wastewater treatment plant (WWTP). In this ecosystem Tubificidae were inoculated, and then adhered to the outer layers of carrier materials in an oxidation tank. During the long-term treatment of sewage volumes of 20,000 m 3 d −1 , the excess sludge production rate was reduced from 0.21 to 0.051 kg m −3 and sludge settleability was significantly improved. When the influent concentrations of COD, NH 4 + –N, PO 4 − –P, and SS were in the ranges of 130.0–459.0 mg L −1 , 14.2–27.5 mg L −1 , 1.6–7.0 mg L −1 , and 60.0–466.0 mg L −1 , respectively, the COD and SS removal efficiency was increased by 8.7% and 13.6% within the symbiotic system compared to the control without Tubificidae. In addition, NH 4 + –N and phosphorus removal efficiency can also be improved. The results showed that both sludge reduction and nutrient removal were enhanced simultaneously significantly within the system utilizing the symbiotic interactions of Tubificidae and microorganisms.

In this study, sequencing batch reactors (SBRs) were used to enrich for dense cultures of nitrifying bacteria. The cultivation conditions of nitrifying bacteria in activated sludge systems will directly affect the nitrogen and other nutrients removal efficiency and the efficient and stable operation of the system. Therefore, take SBRs as the carrier, by cultivating the activated sludge, which were taken from the secondary settling pond of a sewage treatment plant, the number of the heterotrophic bacteria in the sludge decrease while that of the nitrobacteria which become the predominant bacteria increase. The result showed that the enrichment of nitrifying bacteria is feasible under the appropriate pH, temperature, DO and other conditions, and the system of NH 4 +-N removal rate of more than 98%, nitrification rate improved 3 times than that before enrichment.

In animal cells, myo-inositol is an important regulatory molecule in several physiological and biochemical processes, including signal transduction and membrane biogenesis. However, the fundamental biological functions of myo-inositol are still far from clear in plants. Here, we report the genetic characterization of three Arabidopsis thaliana genes encoding d-myo-inositol-3-phosphate synthase (MIPS), which catalyzes the rate-limiting step in de novo synthesis of myo-inositol. Each of the three MIPS genes rescued the yeast ino1 mutant, which is defective in yeast MIPS gene INO1, and they had different dynamic expression patterns during Arabidopsis embryo development. Although single mips mutants showed no obvious phenotypes, the mips1 mips2 double mutant and the mips1 mips2 mips3 triple mutant were embryo lethal, whereas the mips1 mips3 and mips1 mips2+/− double mutants had abnormal embryos. The mips phenotypes resembled those of auxin mutants. Indeed, the double and triple mips mutants displayed abnormal expression patterns of DR5:green fluorescent protein, an auxin-responsive fusion protein, and they had altered PIN1 subcellular localization. Also, membrane trafficking was affected in mips1 mips3. Interestingly, overexpression of PHOSPHATIDYLINOSITOL SYNTHASE2, which converts myo-inositol to membrane phosphatidylinositol (PtdIns), largely rescued the cotyledon and endomembrane defects in mips1 mips3. We conclude that myo-inositol serves as the main substrate for synthesizing PtdIns and phosphatidylinositides, which are essential for endomembrane structure and trafficking and thus for auxin-regulated embryogenesis.

Biosorption of heavy metals from simulated wastewater and the raw electroplating wastewater with “BM (Biosorption of Metals) bacteria” were investigated in this study. The influence of initial pH, biosorbents dose, concentration of ions, contact time and temperature on biosorption capacity of Cr(VI) and Ni(II) were studied. The optimum pH for biosorption of Cr(VI) was found to be low, and the removal efficiency of Cr(VI) was 98.60% with “BM bacteria” at pH 2. The removal efficiency of Ni(II) was increased with increasing the pH, and was enhanced up to 115% compared with the wastewater without BM bacteria. In this experiment, the “BM bacteria” efficiently removed Cu(II), Ni(II), Cr(VI), Zn(II) and COD from the raw electroplating wastewater, and the removal efficiencies were 98.92%, 99.92%, 99.86%, 99.93% and 45.20% respectively.

Based on the fully coupled activated sludge model (FCASM), the novel model Tubificidae ‐Fully Coupled Activated Sludge Model‐hydraulic (T‐FCASM‐Hydro), has been developed in our previous work. T‐FCASM‐Hydro not only describe the interactive system between Tubificidae and functional microorganisms for the sludge reduction and nutrient removal simultaneously, but also considere the interaction between biological and hydraulic field, After calibration and validation of T‐FCASM‐Hydro at Zhuji Feida‐hongyu Wastewater treatment plant (WWTP) in Zhejiang province, T‐FCASM‐Hydro was applied for determining optimal operating condition in the WWTP. Simulation results showed that nitrogen and phosphorus could be removed efficiently, and the efficiency of NH4+‐N removal enhanced with increase of DO concentration. At a certain low level of DO concentration in the aerobic stage, shortcut nitrification‐denitrification dominated in the process of denitrification in the novel system. However, overhigh agitation (>6 mg⋅L−1)...

Activation of washed human platelets initiated with alpha-thrombin, SFLLRN, or AYPGKF invariably results in the generation of PAR-1-(1-41) and PAR-4-(1-47). PAR-1-(1-41) and PAR-4-(1-47) are amino-terminal peptides generated when PAR-1 and -4 are cleaved in their first extracellular domains after R(41) and R(47), respectively, to expose the tethered ligand domains of PAR-1 and -4. Since soybean trypsin inhibitor decreases generation of PAR-1-(1-41) and PAR-4-(1-47) and other platelet aggregation-related responses to these three agonists, but does not inactivate alpha-thrombin, a platelet trypsin-like proteinase apparently activates PAR-1 and -4 to propagate PAR-dependent platelet responses. This study identified the signaling pathways implicated in the generation of the platelet proteinase that in turn produces PAR-1-(1-41) and PAR-4-(1-47), to thereby drive the subsequent PAR-dependent platelet aggregation-related responses to alpha-thrombin, SFLLRN, or AYPGKF. Only inhibitors of signaling enzymes that prevented ATP release (forskolin, PGE(1), or BIMI-1) prevented or delayed the generation of PAR-1-(1-41) and PAR-4-(1-47) in response to all three agonists. SBTI prevented platelet aggregation initiated by alpha-thrombin, SFLLRN, or AYPGKF but did so less effectively when it was added 10 s after each agonist. Thus, the platelet-derived proteinase acts within 10 s of each agonist addition to generate PAR-1-(1-41) and PAR-4-(1-47). Furthermore, alpha-thrombin may not effectively catalyze PAR-1-(1-41) and PAR-4-(1-47) generation. We propose that unidentified ATP-dependent phosphorylation reactions catalyzed by PKC help to generate the platelet-derived proteinase that propagates human platelet PAR-1 and -4 activation by the three agonists.

We previously demonstrated that human platelets activated with SFLLRN release PAR-1 activation peptide, PAR-1-(1-41), even in the presence of hirudin. This observation suggests that during their activation, platelets generate a protease that activates PAR-1. In this study, PAR-1 and -4 activation peptides were detected 10 s afteror=1.0 nm alpha-thrombin, 10 microm SFLLRN, or 100 microm AYPGKF were added to platelets. When SFLLRN or AYGPKF were added to platelets, generation of PAR-1 and -4 activation peptides was complete at 10 s. Generation of both PAR-1 and -4 activation peptides in response to 1 nm alpha-thrombin was significantly inhibited by affinity-purified anti-PAR-1-(35-62) IgY, anti-PAR-4-(34-54) IgY, and by the specific PAR-1 antagonist BMS 200261, but not by the PAR-4 antagonist YD3. Effective inhibition of platelet aggregation in response to 1.0 nm alpha-thrombin occurred only in the presence of both anti-PAR span antibodies. We conclude that platelet activation initiated withor=1.0 nm alpha-thrombin proceeds via simultaneous PAR-1 and -4 activation. Inhibiting the activation of either PAR inhibits activation of the other. Both PAR-1 and -4 activation must be inhibited to prevent platelet activation subsequent to thrombin binding to platelets. The more efficient generation of PAR activation peptides by platelets activated with SFLLRN or AYGPKF, compared with alpha-thrombin, indicates that a platelet-derived serine protease that is inactivated by soybean trypsin inhibitor propagates PAR-1 and -4 activation.

Protease-activated receptor-1 (PAR-1) is a G-protein-linked receptor on platelets and perivascular cells activated by α-thrombin and the PAR-1-activating peptide, SFLLRN. α-Thrombin activates PAR-1 by cleaving it at R41–S42 to release the 41-residue peptide TR(1–41). Unexpectedly, platelet activation with SFLLRN was also associated with PAR-1 cleavage and the release of TR(1–41). Both PAR-1 cleavage and platelet activation resulting from SFLLRN addition to platelets were markedly inhibited by the serine protease inhibitor 4,2-(aminoethyl)-benzene sulphonylfluoride·HCl (pefabloc SC) and soybean trypsin inhibitor, but not by inhibitors of calpain, cysteine proteases or metalloproteases. Thus, a trypsin-like platelet protease propagates SFLLRN-dependent PAR-1 cleavage and platelet activation.