Pollution source identification and abatement for water quality sections in Huangshui River basin, China.

Accurately obtaining the pollution sources and their contribution rates is the basis for refining watershed management. Although many source analysis methods have been proposed, a systematic framework for watershed management is still lacking, including the complete process of pollution source identification to control. We proposed a framework for identification and abatement of pollutants and applied in the Huangshui River Basin. A newer contaminant flux variation method based on a one-dimensional river water quality model was used to calculate the contribution of pollutants. The contributions of various factors to the over-standard parameters of water quality sections at different spatial and temporal scales were calculated. Based on the calculation results, corresponding pollution abatement projects were developed, and the effectiveness of the projects was evaluated through scenario simulation. Our results showed that the large scale livestock and poultry farms and sewage treatment plants were the largest sources of total nitrogen (TP) in Xiaoxia bridge section, with contribution rates of 46.02% and 36.74%, respectively. Additionally, the largest contribution sources of ammonia nitrogen (NH3-N) were sewage treatment plants (36.17%) and industrial sewage (26.33%). Three towns that contributed the most to TP were Lejiawan Town (14.4%), Ganhetan Town (7.3%) and Handong Hui Nationality town (6.6%), while NH3-N mainly from the Lejiawan Town (15.9%), Xinghai Road Sub-district (12.4%) and Mafang Sub-district (9.5%). Further analysis found that point sources in these towns were the main contributor to TP and NH3-N. Accordingly, we developed abatement projects for point sources. Scenario simulation indicated that the TP and NH3-N could be significantly improved by closing down and upgrading relevant sewage treatment plants and building facilities for large scale livestock and poultry farms. The framework adopted in this study can accurately identify pollution sources and evaluate the effectiveness of pollution abatement projects, which is conducive to the refined water environment management.

Corrigendum to "Yiqi Huayu Jiedu Decoction Inhibits the Invasion and Metastasis of Gastric Cancer Cells through TGF-ß/Smad Pathway".

[This corrects the article DOI: 10.1155/2017/1871298.].

ß-Asarone Increases Chemosensitivity by Inhibiting Tumor Glycolysis in Gastric Cancer.

ß-asarone is the main active ingredient of the Chinese herb Rhizoma Acori Tatarinowii, which exhibits a wide range of biological activities. It was confirmed to be an efficient cytotoxic agent against gastroenteric cancer cells. However, the exact mechanism of ß-asarone in gastric cancer (GC) remains to be elucidated. The present study showed the inhibitory effect of ß-asarone on three types of different differentiation stage GC cell lines (MGC803, SGC7901, and MKN74) in a dose-dependent manner. Meanwhile, the synergistic sensitivity of ß-asarone and cisplatin was confirmed by using the median-effect principle. Flow cytometry assay revealed that under both normoxia and CoCl2-induced hypoxia conditions, ß-asarone can induce apoptosis of GC cells, which can block GC cells in the cell cycle G2/M phase, showing obvious subdiploid peak. Moreover, the activity of lactic dehydrogenase (LDH), an enzyme that plays an important role in the final step of tumor glycolysis, was significantly decreased in GC cells following treatment with ß-asarone. Mechanistically, ß-asarone can reduce pyruvate dehydrogenase kinase (PDK) 1, phospho(p)-PDK1, PDK4, hypoxia-inducible factor 1-α (HIF1α), c-myc, STAT5, and p-STAT5 expression, which revealed how ß-asarone affects tumor glycolysis. In conclusion, the present study provided evidence in support of the hypothesis that the increase of chemotherapy sensitization by ß-asarone is associated with the inhibition of tumor glycolysis.

A highly sensitive and selective fluorescence biosensor for hepatitis C virus DNA detection based on δ-FeOOH and exonuclease III-assisted signal amplification.

Developing the high selectivity and sensitivity strategy for nucleic acid detection is crucial for early diagnosis and therapy of diseases. In this work, a novel low back-ground fluorescent sensor platform for the detection of nucleic acid has been developed based on δ-FeOOH nanosheets integrating with exonuclease III-assisted target-recycling signal amplification. Because of the strong binding ability between the single-strand DNA (ssDNA) and the δ-FeOOH nanosheets, the dye-labeled ssDNA probe would be quenched by δ-FeOOH nanosheets through fluorescence resonance energy transfer (FRET). By using magnetic separate properties of δ-FeOOH, the background signal was separated from the sensor system, and the low background sensor system was obtained. After adding the target DNA, a double-strand DNA complex (dsDNA) would be formed between the target DNA and dye-labeled ssDNA probe. Then, the dye-labeled ssDNA probe in the dsDNA complex would be stepwise hydrolyzed into short fragments from 3'-terminus by Exonuclease III, and the fluorescence signal was recovered due to the weak bind affinity between the short fragments and δ-FeOOH nanosheets. By using the fluorescence quenching ability of δ-FeOOH nanosheets and enzyme-assisted target-recycling signal amplification, this strategy could show an excellent selectivity toward hepatitis C virus DNA with a low detection limit of 10 pM. By simply changing the dye-labeled ssDNA probe sequence, this sensing platform can be developed as a universal approach for the simple, sensitive, and selective detection of different target DNA.

A high sensitivity background eliminated fluorescence sensing platform for hyaluronidase activity detection based on Si QDs/HA-δ-FeOOH nanoassembly.

Using fluorescent sensors for highly sensitive and selective detection of biomolecules is a very important strategy in clinical diagnoses as well as biomedical applications. But fluorescent sensors usually suffer from high background signal, which greatly hinders their detection sensitivity. In this work, a novel background-eliminated fluorescence assay for sensitive and selective detection of biomolecule has been developed by coupling feroxyhyte nanosheets (δ-FeOOH) with amino-functionalized silicon quantum dot (Si QDs). We select hyaluronidase (HAase) as the modal target to verify the concept. Si QDs/HA-δ-FeOOH nanoassembly was fabricated by self-assembly of positive Si QDs together with negative HA-δ-FeOOH through electrostatic adsorption. By the introduction of hyaluronidase, the nanoassembly exhibits obviously fluorescence signal recovered. Research suggests that under optimized conditions, this strategy exhibits a good linear response to the concentration of HAase in the range of 0.1 to 12 ng/mL. The detection limit for HAase was 0.02 ng/mL (based on 3σ/S), which was three-order lower than most of the reported fluorescence biosensors for the detection of HAase. Furthermore, this new biosensor has already been applied in the study of urine samples, and the detection results were consistent with those obtained by the clinical tests.

Yiqi Huayu Jiedu Decoction Inhibits the Invasion and Metastasis of Gastric Cancer Cells through TGF-ß/Smad Pathway.

Background. Yiqi Huayu Jiedu Decoction (YHJD) can obviously improve the quality of life of those patients with gastric cancer and prolong their survival. Methods. In vitro experiments, we observe YHJD's effect on the cells' proliferation by MTT assay. Cell adhesion assay, wound-healing assay, and Transwell invasion assay serve to detect its influence on cells' adhesion, migration, and invasion, respectively. Inhibitor (10 µM/L of SB431542) and activator (10 ng/mL of TGF-ß) of TGF-ß/Smad pathway were used to estimate whether YHJD's impact on the biological behavior of gastric cancer cells was related to TGF-ß/Smad pathway. In in vivo studies, YHJD was administered to the nude mice transplanted with gastric cancer to observe its effect on the tumor. Western blotting and immunohistochemical assay were used to test relevant cytokines of TGF-ß/Smad pathway and epithelial-mesenchymal transition (EMT) in MGC-803 cells and the tumor bearing nude mice. Results. YHJD inhibited proliferation, adhesion, migration, and invasion of MGC-803 gastric cancer cells in vitro. In in vivo studies, YHJD reduced the volume of the transplanted tumors. It also enhanced the expression of E-cadherin and decreased the levels of N-cadherin, TGF-ß, Snail, and Slug in both MGC-803 cells and the transplanted tumor by western blot assay. The immunohistochemical assay revealed that YHJD raised E-cadherin in the tumors of the mice; on the contrary, the expression of N-cadherin, Twist, vimentin, TGF-ßR I, p-Smad2, p-Smad3, Snail, and Slug reduced. Conclusion. YHJD can effectively inhibit the invasion and metastasis of gastric cancer cells. The mechanism may be related to TGF-ß/Smad pathway.

Compound Wumei Powder Inhibits the Invasion and Metastasis of Gastric Cancer via Cox-2/PGE2-PI3K/AKT/GSK3ß/ß-Catenin Signaling Pathway.

To explore the role of CWP in invasion and migration of gastric cancer cells and its underlying molecular mechanism, we performed the experiment in SGC-7901 cells both in vitro and in vivo. In the cell experiment, we evaluated cell proliferation by MTT assay. The results showed that CWP can inhibit the growth of SGC-7901 cells. The influence on cell migration and invasion was detected by wound-healing and Transwell invasion assays. The results showed that the abilities of invasion and migration are restrained in CWP group. Western blot showed that CWP can decrease the expression of Cox-2 and inhibit the PI3K/AKT/GSK3ß/ß-catenin signaling pathway. In the animal experiment, we observed that CWP had an inhibitory effect on the growth of xenograft tumors of nude mice. IHC assay, ELISA, RT-PCR assay, and Western blot assay were used to test relevant cytokines of Cox-2/PGE2-PI3K/AKT/GSK3ß/ß-catenin pathway. The results showed that CWP can suppress relevant cytokines of Cox-2/PGE2-PI3K/AKT/GSK3ß/ß-catenin pathway. In conclusion, we suggest that CWP inhibits the invasion and metastasis of SGC-7901 cells via Cox-2/PGE2-PI3K/AKT/GSK3ß/ß-catenin signaling pathway.

A TiS2 nanosheet enhanced fluorescence polarization biosensor for ultra-sensitive detection of biomolecules.

Development of new strategies for the sensitive and selective detection of ultra-low concentrations of specific cancer markers is of great importance for assessing cancer therapeutics due to its crucial role in early clinical diagnoses and biomedical applications. In this work, we have developed two types of fluorescence polarization (FP) amplification assay strategies for the detection of biomolecules by using TiS2 as a FP enhancer and Zn(2+)-dependent self-hydrolyzing deoxyribozymes as catalysts to realize enzyme-catalyzed target-recycling signal amplification. One approach is based on the terminal protection of small-molecule-linked DNA, in which biomolecular binding to small molecules in DNA-small-molecule chimeras can protect the conjugated DNA from degradation by exonuclease I (Exo I); the other approach is based on the terminal protection of biomolecular bound aptamer DNA, in which biomolecules directly bound to the single strand aptamer DNA can protect the ssDNA from degradation by Exo I. We select folate receptor (FR) and thrombin (Tb) as model analytes to verify the current concept. It is shown that under optimized conditions, our strategies exhibit high sensitivity and selectivity for the quantification of FR and Tb with low detection limits (0.003 ng mL(-1) and 0.01 pM, respectively). Additionally, this strategy is a simple "mix and detect" approach, and does not require any separation steps. This biosensor is also utilized in the analysis of real biological samples, the results agree well with those obtained by the enzyme-linked immunosorbent assay (ELISA).

Nicking endonuclease-assisted signal amplification of a split molecular aptamer beacon for biomolecule detection using graphene oxide as a sensing platform.

Sensitive and selective detection of ultralow concentrations of specific biomolecules is important in early clinical diagnoses and biomedical applications. Many types of aptasensors have been developed for the detection of various biomolecules, but usually suffer from false positive signals and high background signals. In this work, we have developed an amplified fluorescence aptasensor platform for ultrasensitive biomolecule detection based on enzyme-assisted target-recycling signal amplification and graphene oxide. By using a split molecular aptamer beacon and a nicking enzyme, the typical problem of false positive signals can be effectively resolved. Only in the presence of a target biomolecule, the sensor system is able to generate a positive signal, which significantly improves the selectivity of the aptasensor. Moreover, using graphene oxide as a super-quencher can effectively reduce the high background signal of a sensing platform. We select vascular endothelial growth factor (VEGF) and adenosine triphosphate (ATP) as model analytes in the current proof-of-concept experiments. It is shown that under optimized conditions, our strategy exhibits high sensitivity and selectivity for the quantification of VEGF and ATP with a low detection limit (1 pM and 4 nM, respectively). In addition, this biosensor has been successfully utilized in the analysis of real biological samples.

A "turn-on" fluorescent sensor for detection of Pb2+ based on graphene oxide and G-quadruplex DNA.

A rapid, sensitive and selective fluorescence sensor for detection of Pb(2+) was developed based on a Pb(2+)-induced G-quadruplex and graphene oxide. By using a specific G-rich DNA sequence, this strategy provided a promising alternative to Pb(2+) determination in the presence of Hg(2+) escaping from the use of a masking agent of Hg(2+).

Exploring the mechanism of interaction between 5-(ethoxycarbonyl)-6-methyl-4-(4-methoxyphenyl)-3,4-dihydropyrimidin-2(1H)-one and human serum albumin: Spectroscopic, calorimetric and molecular modeling studies.

In this paper, binding interaction of 5-(ethoxycarbonyl)-6-methyl-4-(4-methoxyphenyl)-3,4-dihydropyrimidin-2(1H)-one (EMMD) with human serum albumin (HSA) under physiological conditions was investigated by using spectroscopy, isothermal titration calorimetry (ITC) and molecular modeling techniques. The results of spectroscopic studies suggested that EMMD have a strong ability to quench the intrinsic fluorescence of HSA through static quenching procedure. ITC investigations indicated that drug-protein complex was stabilized by hydrophobic forces and hydrogen bonds, which was consistent with the results of molecular modeling studies. Competitive experiments indicated the displacement of warfarin by EMMD, which revealed that the binding site of EMMD to HSA was located at subdomain IIA.