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In this communication, three novel donor-acceptor-donor type second near-infrared AIE fluorophores based on strong electron-acceptor 2,2'-(anthracene-9,10-diylidene) dimalononitrile have been successfully developed for bioimaging, in which they exhibit good photostability and can be used in mouse ear vessel imaging with high resolution (FWHM = 93.4 μm/SBR = 1.5) after capsuling in nanoparticles with good biocompatibility.

Osteoarthritis (OA) is one of the most painful and widespread chronic degenerative joint diseases and is characterized by destructed articular cartilage and inflamed joints. Previously, our findings indicated that circular RNA ciRS-7 (ciRS-7)/microRNA 7 (miR-7) axis is abnormally expressed in OA, and regulates proliferation, inflammatory responses, and apoptosis of interleukin-1β (IL-1β)-stimulated chondrocytes. However, its underlying role in OA remains unknown. In this study, we first validated cartilage degradation and defection of autophagy in samples of OA patients. IL-1β initially stimulated autophagy of chondrocytes, and ultimately significantly suppressed autophagy. Upregulated ciRS-7/down-regulated miR-7 aggravated IL-1β-induced cartilage degradation, and restrained autophagy in vitro. Gene sequencing and bioinformatics analysis performed on a control group, IL-1β group, and IL-1β+miR-7-mimics group demonstrated that seven of the most significant mRNA candidates were enriched in the interleukin-17 (IL-17) signaling pathway. Increased IL-17A levels were also observed by qRT-PCR and ELISA. In addition, it was revealed that the ciRS-7/miR-7 axis ameliorated cartilage degradation and defection of autophagy by PI3K/AKT/mTOR activation in IL-1β-induced chondrocytes. Furthermore, an OA model was established in rats with medial meniscus destabilization. miR-7-siRNA-expressing lentiviruses alleviated surgical resection-induced cartilage destruction of OA mice, whereas miR-7 mimics worsened the effects. Thus, these findings revealed that the mechanism of the ciRS-7/miR-7 axis involved regulating OA progression and provided valuable directions for OA treatment.

In this work, α-MoO3 and h-MoO3 are synthesized by a simple hydrothermal method. Under ambient conditions, α-MoO3 has a high catalytic wet air oxidation (CWAO) activity for methylene blue (MB), while h-MoO3 has no activity: 64% of MB can be degraded after 20 min. When adding an additional man-made light source, the performances of h-MoO3 and α-MoO3 remain almost unchanged. However, with elevating the reaction temperature from 25 to 40 °C, the activity has not been improved for h-MoO3, while the activity of α-MoO3 also has no improvement from 25 to 35 °C. When the temperature rises to 40 °C, the performance of α-MoO3 improved significantly: the degradation percentage reaches 90% after 20 min. Crystal structure analysis results show that the activity of α-MoO3 originates from Jahn–Teller distortion of the [MoO6] octahedron, resulting in the formation of Lewis acid sites. Furthermore, H2-temperature programmed reduction (H2-TPR) and O2-temperature programmed desorption (O2-TPD) results indicate that α-MoO3 has a higher lattice oxygen mobility and a higher oxidization ability than h-MoO3. This ambient CWAO process is energy-saving and low-cost, which is promising for indoor clearance.

Hydrogen peroxide (H2O2), one of the reactive oxygen species (ROS), plays vital roles in diverse physiological processes. Thus, herein, to improve the signal-to-noise ratio, a new near-infrared region (NIR) fluorophore (PCN) based on reduced phenazine was developed. PCN was further designed as a "turn on" fluorescent probe (PCN-BP) for the detection of H2O2 by introducing p-boratebenzyl. After H2O2 was added, the p-boratebenzyl group in PCN-BP was oxidized to p-hydroxy benzyl; it then self-departed, forming PCN, which displayed 24-fold NIR emission at 680 nm with a large Stokes shift (more than 200 nm). This probe presented an excellent linear relation with the concentration of H2O2 and good selectivity to various ions, ROS and biothiols; thus, it can be utilized as a colorimetric and fluorescence turn-on probe. More importantly, the probe was also employed for the exogenous and endogenous imaging of H2O2 in RAW 264.7 cells.

Organic small-molecule fluorophores with near-infrared IIa (NIR-IIa) emission have great potential in pre-clinical detection and inoperative imaging due to the high-spatial resolution and deep penetration. However, developments of the NIR-IIa fluorophores are still facing considerable challenges. In this work, a series of diketopyrrolopyrrole (DPP)-based fluorophores were designed and synthesized. Subsequently, nanomaterial T25@F127 with significant NIR-IIa emission properties was rationally prepared by encapsulating DPP-based fluorophore T25, and was selected for fluorescence angiography and cerebral vascular microscopic imaging with nearly 800 μm penetrating depth and excellent signal-background ratio of 4.07 and 2.26 (at 250 and 400 μm), respectively. Furthermore, the nanomaterial T25@cRGD with tumor targeting ability can image tiny metastatic tumor on intestine with a small size of 0.3 mm×1.0 mm and high-spatial resolution (SBR=3.84). This study demonstrates that the nanomaterials which encapsulated T25 behave as excellent NIR-IIa fluorescence imaging agents and have a great potential for in vivo biological application.

In this work, we mainly investigate the influence of structure water on crystal structure, electronic structure, band structure, and charge separation of WO3·2H2O. It is found, for the first time, that although water is a weak electron donor, a ligand-to-metal charge transfer (LMCT) from H2O to W occurs. The structure water contributes to the conduction band (CB) of WO3·2H2O, and the band gap of WO3·2H2O is obviously narrowed, thus increasing the light absorption obviously. Moreover, the results of EIS, photocurrent spectra, and PL show that structure water in WO3·2H2O also improves the charge separation and transfer efficiency of the catalyst. This is the first investigation on the LMCT transfer from structure water (a weak electron donor) to tungsten, which obviously improves light absorption and charge separation. Under visible light irradiation (λ ≥ 420 nm), WO3·2H2O nanosheets have a photocatalytic activity 2.3 times higher than that of WO3 for the degradation of methylene blue (MB). The kind number of photochemical materials can be increased greatly, because structure water-contained compounds widely exist in nature.

So far, BiOF nanodisks exposed with {101} facets have not been reported. In this work, BiOF mainly exposed with {101} facets, instead of common {001} facets, are synthesized at different pH values via a simple hydrothermal method. It is interesting that BiOF thick rectangular plates and thin round nanodisks are formed through the growth preferential along [001] and [101] directions, respectively. On the base of layered crystallography structure, the preferential growth along [001] direction favors to form a thick multi-layered structure, whereas [101] direction for a thin fewer-layered structure. Moreover, more surface oxygen vacancies are contained in thin nanodisks, which reduces the band gap and improves charge transfer and separation. As a result, BiOF round nanodisks show an activity 7.9 times higher than rectangular plates for the degradation of rhodamine B (RhB) under ultraviolet light irradiation (λ ≤ 400 nm).

Background and purpose Non-small-cell lung cancer (NSCLC) accounts for up to 80-85% of all lung cancers and has a disappointing prognosis. Flavonoids exert anticancer properties, mostly involving stimulation of ROS production without significant toxicity to normal cells. This study was aimed to delineate the effect of diosmetin, a natural flavonoid, on NSCLC cells and its ability to enhance the antitumour activity of paclitaxel. Experimental approach NSCLC cells, normal cell lines HLF-1 and BEAS-2B, and immunodeficient mice were chosen as models to study the effects of diosmetin. Changes in cell viability, apoptosis, and ROS were analysed by MTT assay, flow cytometry assay, and fluorescent probe DCFH-DA. Expression of proteins and mRNA was determined by Western blotting and real-time RT-PCR. Growth of xenografted tumours was measured. Spleens and other vital organs were analysed with histological and immunohistochemical techniques. Key results Diosmetin induced selective apoptotic death in NSCLC cells but spared normal cells, via ROS accumulation. Diosmetin induced ROS production in NSCLC cells probably via reducing Nrf2 stability through disruption of the PI3K/Akt/GSK-3β pathway. The in vitro and in vivo xenograft studies showed that combined treatment of diosmetin and paclitaxel synergistically suppressed NSCLC cells. Histological analysis of vital organs showed no obvious toxicity of diosmetin, which matched our in vitro findings. Conclusions and implications Diosmetin selectively induced apoptosis and enhanced the efficacy of paclitaxel in NSCLC cells via ROS accumulation through disruption of the PI3K/Akt/GSK-3β/Nrf2 pathway. Therefore, diosmetin may be a promising candidate for adjuvant treatment of NSCLC.

Intracellular reactive oxygen species is involved in a wide variety of physiological and pathological processes. In this work, we have developed a new mitochondria-targeting probe (DPP-S) for superoxide anion detection with ratiometric fluorescence response. DPP-S exhibited an obvious color change from violet to orange along with a distinct fluorescence change with maximum emission peak from 652 to 545 nm in response to superoxide anion. The limit of detection of DPP-S for superoxide anion was calculated to be 20.5 nM. Imaging studies taken in MCF-7 and RAW264.7 cells showed that DPP-S could be employed as a ratiometric fluorescent probe for endogenous superoxide anion detection and imaging in living cells with a large emission shift. Furthermore, the colocalization study indicated that DPP-S can localize in mitochondria specifically. Finally, the fluorescent probe was successfully applied for superoxide anion imaging in mice.

With the increasing shortage of petroleum-based resources, the exploitation and application of the polymers derived from the renewable resources has becomes increasingly important for the industrial development. In this work, in order to promote the direct application of tung oil in the coating field, the tung oil-based polymers with the excellent mechanical properties by using cationic photoinitiator as the “green” initiator were prepared. The cationic polymerization mechanism and the optimal polymerization conditions of methyl eleostearate (ME) induced by triarylsulfonium salt (TAS) are characterized via the nuclear magnetic resonance spectroscopy. The effects of different monomers on the properties of tung oil-based polymers and the post curing behaviors of the polymers are studied by dynamic mechanical test and microtensile test. The results display that the heating treatment after UV irradiation is necessary and favorable for the cationic polymerization of ME induced by TAS. And the optimal reaction condition is 500 W of irradiation energy, 5 wt% of initiator concentration, 60 min of irradiation time, 100 °C of heating temperature and 3 h of heating time. Moreover, tung oil-based polymers with good hydrophobicity can be obtained under the optimal reaction condition. In addition, adding 20 wt% divinylbenzene and 10 wt% styrene to the tung oil can effectively increase the mechanical properties and glass transition temperatures (Tg) of tung oil-based polymers.

Donor–acceptor (D–A) type conjugated organic polymers exhibited great potential for photocatalytic hydrogen evolution due to their diverse synthetic approaches, tunable energy band, and electronic structure. But the poor dispersion of most conjugated organic polymers limited their photocatalytic performance. Herein, we designed and developed a series of D–A type conjugated organic polymers with benzene as the donor and diketopyrrolopyrrole (DPP) with different side chains on N sites as the acceptor. We changed the length of the side chain and further introduced oxygen atoms on side chains. As a result, the hydrogen evolution rate (HER) of PDPP3B-O4 with a short butoxy chain as the side chain was 5.53 mmol h−1 g−1 with 1 wt% Pt loading (λ > 400 nm), which increased 110 times compared to PDPP3B-C8 with a long octyl chain. All polymers showed outstanding photocatalytic stability. Notably, an apparent quantum yield (AQY) of 5.7% at 450 nm was achieved by PDPP3B-O4, and even a still high AQY of 1.13% at 600 nm was obtained due to its excellent light capture capability. PDPP3B-O4 showed a superior photocatalytic performance because of the wider absorption spectrum and better wettability via side chain engineering.

Fluorescent biosensors with aggregation-induced emission (AIE) have received much attention in the field of bioimaging and therapeutic applications. Although the side chains of AIE sensors have important impacts on the optical performance, imaging and therapy, only a few studies were emphasized on side chain effects compared to the well-established fluorescent backbone systems. In this work, a series of turn-on near-infrared (NIR) pyridinium-functionalized dibenzo[a,c]phenazine salt fluorescent probes (BD2C/BD8C/BD16C) possessing ethyl, octyl and hexadecyl chains were designed and facilely synthesized, and the influence of the alkyl chain length on their optical properties, lipopolysaccharide (LPS) detection and singlet-oxygen quantum yield were systematically investigated. The homologs can exhibit both promising AIE properties and desirable large Stokes shift (ca. 190 nm). Owing to the electrostatic interactions between the two oppositely charged species, the probe with pyridine salt of positive charge could efficiently aggregate with the negatively charged LPS. By reducing the alkyl chain length, BD2C toward LPS showed significant fluorescence enhancement with a relatively low detection limit (2.6 × 10−8 M). Additionally, the singlet oxygen yield of BD2C also showed a significant improvement (70.6%) compared to BD8C and BD16C (30.7% and 30.2%, respectively). The amphiphilic BD2C bearing ethyl chain and positively charged pyridinium salt can embed into the bacterial membrane, thus increasing the membrane permeability and causing dark toxicity. Furthermore, BD2C can also serve as an effective antibacterial photosensitizer under 530 nm light irradiation by inducing reactive oxygen species (ROS) generation which is a rarely reported example to date.

Background: MiR-7 has been recognized as a promoting factor of osteoarthritis (OA), but the specific down-stream pathway of miR-7 still remains unknown. Further investigation of the molecular regulatory mechanism of miR-7 might help develop a novel therapeutic method for OA.Results: Here we revealed that Semaphorin 6D (SEMA6D) was a direct target gene of miR-7, of which presented a negatively regulatory relation in vitro and in vivo. Lucubration of SEMA6D suggested that SEMA6D is validated to promote the anabolic metabolism and reduce the catabolism of chondrocytes via inhibiting the activation of p38 pathway.Conclusions: Present research illustrated that SEMA6D is a negatively regulatory factor of miR-7 and a pivotal mediator of the catabolism and anabolism of chondrocytes. SEMA6D exerts its function via inhibiting the activation of p38 pathway.

Platelet-derived growth factor receptors (PDGFRs) are abundantly expressed by stromal cells in the non-small cell lung cancer (NSCLC) microenvironment, and in a subset of cancer cells, usually with their overexpression and/or activating mutation. However, the effect of PDGFR inhibition on lung cancer cells themselves has been largely neglected. In this study, we investigated the anticancer activity of CP-673451, a potent and selective inhibitor of PDGFRβ, on NSCLC cell lines (A549 and H358) and the potential mechanism. The results showed that inhibition of PDGFRβ by CP-673451 induced a significant increase in cell apoptosis, accompanied by ROS accumulation. However, CP-673451 exerted less cytotoxicity in normal lung epithelial cell line BEAS-2B cells determined by MTT and apoptosis assay. Elimination of ROS by NAC reversed the CP-673451-induced apoptosis in NSCLC cells. Furthermore, CP-673451 down-regulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) probably through inhibition of PI3K/Akt pathway. Rescue of Nrf2 activity counteracted the effects of CP-673451 on cell apoptosis and ROS accumulation. Silencing PDGFRβ expression by PDGFRβ siRNA exerted similar effects with CP-673451 in A549 cells, and when PDGFRβ was knockdowned by PDGFRβ siRNA, CP-673451 produced no additional effects on cell viability, ROS and GSH production, Nrf2 expression as well as PI3K/Akt pathway activity. Specifically, Nrf2 plays an indispensable role in NSCLC cell sensitivity to platinum-based treatments and we found that combination of CP-673451 and cisplatin produced a synergistic anticancer effect and substantial ROS production in vitro. Therefore, these results clearly demonstrate the effectiveness of inhibition of PDGFRβ against NSCLC cells and strongly suggest that CP-673451 may be a promising adjuvant chemotherapeutic drug.

Superoxide anion ( O 2 •- ), as a kind of crucial reactive oxygen species (ROS), often causes a series of oxidative damage and various biological dysfunction when it is excessive in cells. Compared with other detection methods, fluorescence detection is often used for cell imaging due to its high temporal and spatial resolution. Hence, a novel “turn-on” fluorescent probe DMPS-O based on N,N-dimethylaniline as a donor and pyridinium group as an acceptor was designed and synthesized to detect superoxide anion. DMPS-O showed a remarkable fluorescence enhancement in the near-infrared region and a large Stokes shift after reacting with superoxide anion and its limit of detection was calculated to be 22.2 nM. Finally, CCK-8 and confocal fluorescence imaging experiments revealed that the fluorescent probe DMPS-O with low cytotoxicity was suitable for detecting endogenous superoxide anions and locating mitochondria in the MCF-7 and HepG2 cells.

Diabetic nephropathy (DN) is characterized by proliferation of mesangial cells, mesangial hypertrophy and extracellular matrix (ECM) accumulation. Our recent study found that andrographolide inhibited high glucose-induced mesangial cell proliferation and fibronectin expression through inhibition of AP-1 pathway. However, whether andrographolide has reno-protective roles in DN has not been fully elucidated. Here, we studied the pharmacological effects of andrographolide against the progression of DN and high glucose-induced mesangial dysfunction. Diabetes was induced in C57BL/6 mice by intraperitoneal injection of streptozotocin (STZ). After 1 weeks after STZ injection, normal diet was substituted with a high-fat diet (HFD). Diabetic mice were intraperitoneal injected with andrographolide (2 mg/kg, twice a week). After 8 weeks, functional and histological analyses were carried out. Parallel experiments uncovering the molecular mechanism by which andrographolide prevents from DN was performed in mesangial cells. Andrographolide inhibited the increases in fasting blood glucose, triglyceride, kidney/body weight ratio, blood urea nitrogen, serum creatinine and 24-h albuminuria in diabetic mice. Andrographolide also prevented renal hypertrophy and ECM accumulation. Furthermore, andrographolide markedly attenuated NOX1 expression, ROS production and pro-inflammatory cytokines as well. Additionally, andrographolide inhibited Akt/NF-κB signaling pathway. These results demonstrate that andrographolide is protective against the progression of experimental DN by inhibiting renal oxidative stress, inflammation and fibrosis.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with a disappointing prognosis. The aim of this study was to investigate the anticancer effect of sesamin and the underlying mechanism. The MTT assay was used to detect the proliferation of NSCLC cells. The cell cycle and apoptosis were analyzed by flow cytometry. The protein levels of Akt, p-Akt (Ser473), p53, cyclin D1, CDK2, MDM2, p-MDM2 (Ser166) were detected by western blotting. The expression of p-Akt (Ser473), p53 and Ki67 in vivo was analyzed by IHC. Histopathologic analyses of major organs (heart, liver, spleen, lung and kidney) were performed by H&E staining. The results show that sesamin suppressed cell proliferation and induced apoptosis of NSCLC cells (A549 and H1792) in a dose-dependent manner. Treatment with sesamin caused cell cycle arrest at G1 phase and inhibited cyclin D1 and CDK2 expression. In addition, sesamin inhibited Akt activity and upregulated p53 expression both in vivo and in vitro. When Akt and p53 were suppressed by LY294002 and PFTα, respectively, sesamin exerted no additional effects. The in vivo results mostly matched the in vitro findings. Specifically, sesamin exerted little damage to major organs. Taken together, this study demonstrates that sesamin suppresses NSCLC cell proliferation by induction of G1 phase cell cycle arrest and apoptosis via Akt/p53 pathway. Therefore, sesamin may be a promising adjuvant treatment for NSCLC therapy.

M2-type tumor-associated macrophages (TAMs) infiltration contributes to cancer malignant progression. However, the mechanisms for controlling recruitment and M2 polarization of macrophages by cancer cells are largely unclear. NADPH oxidase 4 (NOX4) is abundantly expressed in non-small cell lung cancer (NSCLC) and mediates cancer progression. NOXs are in close relation with cancer-related inflammation, nevertheless, whether tumoral NOXs influence microenvironmental macrophages remains undentified. This study found that there was a close association between NOX4 expression and macrophage chemotaxis in patients with NSCLC analyzed using TCGA RNA-sequencing data. NOX4 in NSCLC cells (A549 and Calu-1 cell lines) efficiently enhanced murine peritoneal macrophage migration and induces M2 polarization. Immunohistochemical analysis of clinical specimens confirmed the positive correlation of NOX4 and CD68 or CD206. The mechanical study revealed that tumoral NOX4-induced reactive oxygen species (ROS) stimulated various cytokine production, including CCL7, IL8, CSF-1 and VEGF-C, via PI3K/Akt signaling-dependent manner. Blockade of the function of these cytokines reversed NOX4 effect on macrophages. Specifically, the results showed that tumoral NOX4-educated M2 macrophages exhibited elevated JNK activity, expressed and released HB-EGF, thus facilitating NSCLC proliferation in vitro. Pretreatment of macrophages with JNK inhibitor blocked tumoral NOX4-induced HB-EGF production in M2 macrophages. Finally, in a xenograft mouse model, overexpression of NOX4 in A549 cells enhanced the tumor growth. Elimination of ROS by NAC or inhibition of NOX4 activity by GKT137831 suppressed tumor growth accompanied by reduction in macrophage infiltration and the percentage of M2 macrophages. In conclusion, our study indicates that tumoral NOX4 recruits M2 TAMs via ROS/PI3K signaling-dependent various cytokine production, thus contributing NSCLC cell growth., Graphical abstract fx1, Highlights • NOX4 has a novel function that affects cancer progression via action on TAM. • There exists a NOX4-dependent crosstalk between NSCLC cells and M2 macrophages. • GKT137831 has anti-cancer potential for targeting cancer microenvironmental TAM.

The cerebellum is extremely sensitive to heat-induced injury because of the abundance of Purkinje cells. This study explored the influence of temperature on cerebellar metabolite levels by magnetic resonance spectroscopy (MRS).Ten healthy volunteers were recruited to undergo a MRS examination in the summer and winter. Twenty-four ordinary patients with fever underwent the same examination during fever and after recovery. All MR spectras were recorded from the cerebellum. Metabolites ratios including N-acetyl aspartate/creatine (NAA/Cr), choline/creatine (Cho/Cr), and N-acetyl aspartate/choline (NAA/Cho) were calculated.There are no significant differences in cerebellar metabolite levels in the 10 healthy volunteers during summer and winter (p .05). For the 24 patients with fever, the cerebellar Cho/Cr ratios during fever were increased compared with those after recovery (p = .043).In summary, MRS plays a role in the evaluation of the influence of temperature on cerebellar metabolite levels. It was observed that cerebellar metabolite levels are not influenced by seasonal temperature but are influenced by body temperature.

Confirmed by the test, the amount of the sulfur defect in CdS is simply controlled by varying the amount of acid added. The concentration of the surface hole has been influenced by the increasing of the sulfur defect. The visible light activity (λ > 420 nm) of 275-CdS (275: adding 275 μL HNO3) is about 1.39 and 1.35 times as high as that of CdS and 400-CdS (400: adding 400 μL HNO3), respectively. The increased concentration of the hole on catalyst surface is the main reason for the improved degradation performance.

From viewpoint of engineering application, to dramatically enhance the photocatalyst performance is the absolute truth for solar energy photocatalysis. Although various modification strategies have been developed to enhance the activity of a photocatalyst, the improvement extent is actually not obvious with a single strategy. In this work, abundant bismuth is used to obtain the Bi-doped TiO2 (Dx), Bi@TiO2 (Sy) and Bi@Bi-doped TiO2 (SyDx) samples. Compared with original TiO2, the activities of Dx and Sy can only increase by 0.26 and 1.9 times under UV light irradiation (λ≤ 400 nm), respectively; however, the degradation activity of S10D1 has increased by 4.5 times, showing an obvious synergistic effect between Mott-Schottky junction and oxygen defect, in which oxygen defect and Mott-Schottky junction obviously expands the light adsorption range and promotes reduces the charge transfer and separation. To the best of our knowledge, the abundant, environmental-friendly bismuth-based Bi@Bi-doped TiO2 has not been reported so far. The simple integration strategy is remarkably efficient to greatly enhance the photocatalytic activity, compared to single strategy.

From the viewpoint of engineering application, it is highly desirable to develop a low-cost, fossil energy–saving degradation technology. In this work, hydrated molybdenum oxide (MoO3·0.55H2O) is prepared by a simple chemical method. It is interesting that under indoor natural ambient conditions, 79% of methylene blue is degraded by hydrated molybdenum oxide after 150 min, but under the same conditions, anhydrous molybdenum oxide does not have any degradation activity. It is found that the outstanding ambient activity of hydrated molybdenum oxide is mainly attributed to the photothermal synergistic effect caused by structure water. On one hand, the coordination of structure water with molybdenum brings about the Jahn–Teller distortion of MoO6 octahedron, giving rise to Lewis acid sites that promote the adsorption and activation of oxygen. O2–temperature-programmed desorption and H2–temperature-programmed reduction profiles show that compared with MoO3, MoO3·0.55H2O has a higher oxygen adsorption ability and a higher oxidation ability. Jahn–Teller effect is mainly responsible for the thermocatalytic activity. On the other hand, the ligand-to-metal charge transfer (LMCT) transfer from structure water to molybdenum obviously increases the light absorption, thus LMCT is mainly responsible for the photocatalytic activity The most important is that compared with conventional photocatalysis, no artificial light source equipment is required; compared with thermocatalysis, no extra heating equipment is needed. Thus, this mild degradation process is low-cost, energy-saving and space-saving, which is very promising for indoor or limited space cleaning.

A new diketopyrrolopyrrole-based fluorescent probe (DPP-AM) was designed and synthesized for ratiometric detection of esterase and for imaging of live and dead cells in different modes. DPP-AM showed red fluorescence because of the intramolecular charge transfer (ICT) process from the DPP moiety to the pyridinium cation and gave remarkable ratio changes (about 70 folds), with the fluorescence changing from red to yellow, after treating with esterase because of the broken ICT process. Besides, the detection limit of DPP-AM toward esterase in vitro was 9.51 × 10–5 U/mL. After pretreating with H2O2 and ultraviolet light radiation, the health status of TPC1 cells was successfully imaged. More importantly, DPP-AM showed yellow fluorescence in live cells and a red fluorescent signal in dead cells, indicating that DPP-AM has great potential applications for assessing esterase activity as well as for discriminating live and dead cells.

Vortioxetine is a multimodal antidepressant that has been recently utilized globally. Vortioxetine hemi-hydrochloride is a novel salt that was previously reported in our research. However, the pharmacokinetics of this salt and the metabolites of Vortioxetine in vivo remain unknown. In this study, the pharmacokinetics of the Vortioxetine hemi-hydrochloride salt is explored in rats through a newly developed ultra-performance liquid chromatography with tandem mass spectrometry method. In addition, ultra-performance liquid chromatography coupled with quadrupole time of flight mass spectrometry was used to identify the metabolites of Vortioxetine in vivo. The results demonstrate that after a single, 3 mg/kg oral dose, the maximum concentration for the Vortioxetine hemi-hydrochloride salt is 14.63 ± 4.00 ng/mL, and is attained in 1.00∼4.00 h. The area under the plasma concentration-time curve from time 0 to 24 h is 67.30 ± 23.78 ng·h·mL-1 . Additionally, 29 metabolites were identified after the oral administration of 10 mg/kg, including 17 metabolites in the plasma, nine in the urine, and 12 in the feces. Eleven metabolites were novel. The major metabolic pathways include methylation, hydroxylation, oxidation, and glucuronidation. In conclusion, this study provides insight for further development of the Vortioxetine hemi-hydrochloride salt.

Glutathione S-transferase A1 (GSTA1) is a phase II detoxification enzyme and serves a crucial role in anti-cancer drug resistance. In our previous study, GSTA1 was identified to be highly expressed in various subtypes of non-small-cell lung cancer cell lines compared with human embryonic lung fibroblast cell line MRC-5. The aim of the present study was to investigate the effect of GSTA1 expression on the proliferation and apoptosis of A549 cells. GSTA1 expression was knocked down or with overexpressed using lentivirus particles. Western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to assess the protein, and mRNA levels of GSTA1 in A549 cells, respectively. The effect of GSTA1 manipulation on cell proliferation and apoptosis were investigated in vitro using MTT assays, Hoechst 33258 staining and flow cytometry, and in vivo using A549 cell line xenografts in nude mice. The results of the western blot analysis and RT-qPCR revealed that stable cell models of GSTA1 knockdown, and overexpression were established. The data of the MTT assay indicated that the downregulation of GSTA1 significantly inhibited cell proliferation compared with si-control-transfected cells. These si-GSTA1 A549 cells exhibited typical morphological changes of apoptosis, including chromatin condensation and shrunken nuclei compared with the si-control counterparts. An AnnexinV-fluorescein isothiocyanate assay verified that the downregulation of GSTA1 significantly induced cell apoptosis in vitro. In addition, overexpression of GSTA1 significantly promoted tumor growth in vivo. Accordingly, downregulation of GSTA1 suppressed tumor growth. In conclusion, GSTA1 plays an important role in regulation of cell proliferation and cell apoptosis in A549 cell line.

The synthesis and biological evaluation of a novel series of compounds based on suberoylanilide hydroxamic acid (SAHA) had been designed as potential histone deacetylase inhibitors (HDACis). Molecular docking studies indicated that our derivatives had better fitting in the binding sites of HDAC8 than SAHA. Compounds 1-5 were synthesized through the synthetic routes. In biological test, compounds also showed good inhibitory activity in HDAC enzyme assay and more potent growth inhibition in human glioma cell lines (MGR2, U251, and U373). A representative compound, N3F, exhibited better inhibitory effect (HDAC, IC50 = 0.1187 μm; U251, IC50 = 0.8949 μm) and lower toxicity for human normal cells (LO2, IC50 = 172.5 μm and MRC5, IC50 = 213.6 μm) compared with SAHA (HDAC, IC50 = 0.8717 μm; U251, IC50 = 8.938 μm; LO2, IC50 = 86.52 μm and MRC5, IC50 = 81.02 μm). In addition, N3F obviously increased Beclin-1 and Caspase-3 and 9 as well as inhibited Bcl-2 in U251 cells. All of our results indicated that these SAHA cap derivatives could serve as potential lead compounds for further optimization. In addition, N3F and N2E both displayed promising profile as antitumor candidates for the treatment of human glioma.

Tumors require nutrients and oxygen for growth and metastasis. Vasculogenic mimicry (VM) has been found as a new manner of blood supply, which is characterized as the formation of tumor cell-lined vessels instead of endothelial vessels. This is why angiogenesis agents targeted to endothelial cells show a limited efficacy. Up to this point, there is no effective drug reported for inhibiting VM formation. Niclosamide is an oral anti-helminthic drug used to treat human tapeworms. Recent studies have indicated that niclosamide has broad applications for cancer and other diseases. In this study, we found that niclosamide could not only inhibit proliferation and promote apoptosis of oral cancer cells, but also inhibited VM formation in vitro and in vivo through downregulation of the expression of VM-related genes VEGFA, MMP2, ROCK1 and Cdc42. In addition, niclosamide upregulated miR-124 and downregulate phosphorylated (p)-STAT3 expression. Further studies showed that, the stable highly expressing miR-124 cell line HN6-miR-124, such as niclosamide, could downregulate p-STAT3 expression. Moreover, HN6-miR‑124 showed lower mobility, invasiveness and VM formation ability than control cells. Taken together, our study suggests that niclosamide functions as a new inhibitor of VM in oral cancer through upregulation of miR-124 and downregulation of STAT3, providing a new and safe potential drug candidate for anti-VM therapy.

The activation of nuclear factor-κB (NF-κB) and the subsequent overexpression of its downstream targets transforming growth factor-β1 (TGF-β1) and fibronectin (FN) are among the hallmarks for the progressive diabetic nephropathy. Our previous studies demonstrated that emodin ameliorated renal injury and inhibited extracellular matrix accumulation in kidney and mesangial cells under diabetic condition. However, the molecular mechanism has not been fully elucidated. Here, we showed that emodin significantly attenuated high glucose-induced NF-κB nuclear translocation in mesangial cells. Interestingly, emodin also inhibited the DNA-binding activity and transcriptional activity of NF-κB. Furthermore, NF-κB-mediated TGF-β1 and FN expression was significantly decreased by emodin. These results demonstrated that emodin suppressed TGF-β1 and FN overexpression through inhibition of NF-κB activation, suggesting that emodin-mediated inhibition of the NF-κB pathway could protect against diabetic nephropathy.

The photolysis and hydrolysis of prallethrin was studied in the laboratory. The result of the test showed that the photolysis reaction of prallethrin in aqueous solutions irradiated by 500w xenon lamp fitted to the first order dynamic equation. The results also showed that the hydrolysis rate of prallethrin in buffer solutions with pH values of 5 in 25C were very slow. The rising temperature and pH values could both accelearate the hyrolysis. And discussion was also conducted to the mechanism of hydrolysis. KEYWORD: Prallethrin; Photolysis; Hydrolysis; Gas Chromatography International Conference on Industrial Technology and Management Science (ITMS 2015) © 2015. The authors Published by Atlantis Press 1752 was used as the light source, and quartz cold well was used to surround the lamp, which could run through the condensed water to keep the stability of the temperature inside the reactor. The photolysis reaction tube was quartz tube, which was 70 mm away from the light source, and the light intensity was 1.05×10 4 Lux. Water samples were taken regularly during the test to determine the changes of the pesticide concentration. During the photolysis test period, any other light resources should be isolated from the photolysis to reduce the influences on the test results. The spectral signature of the xenon lamp used in the test was similar to that of the sunlight (Fig.1), which could ensure that the artificial simulated light degradation conditions were as close to the natural conditions as possible. Fig. 1 The comparison between spectra of xenon lamp and spectra of the sunlight 1.2.5 Analysis of pesticide residues Water extraction: 10mL of water sample was taken and put in the separatory funnel, which was added with 20mL×2 petroleum ether, and after organic phase combination, the rotary evaporator was used to evaporate and concentrate the sample into a certain volume for gas chromatography. The recovery rate of pyrethroids at different pH buffer solutions was 93.4 100%, which showed a 3.03-10% deviation to the standard. Conditions of determination by gas chromatogra phy were as follows: Shimadzu GC-14B gas chromatograph and electron capture detector were used for the gas chromatography. Chromatographic column: the fused silica capillary column with 5% phenyl methyl silicone as the stationary phase and HP-5 length of 30m, diameter of 0.25mm and film thickness of 0.25m. Fig. 2 GC Temperature conditions: column temperature of 220C, vaporizing chamber of 250C, detecting chamber of 250 C. Gas flow rate: nitrogen of 40mL/min. Sample size: 1L. The concentration of pralle thrin standard solution: 25g/mL, as Figure 2 shows. 2 RESULTS AND DISCUSSION 2.1 Hydrolysis characteristics prallethrin The hydrolysis rate of pesticide was subjected to the influence of pesticide properties and water environment conditions, and the hydrolysis of pesticide in buffer solution system was fitted to the first order dynamic equation, which could be expressed using the following formula

Conventional chemotherapy fails to cure metastatic hepatoma mainly due to its high hepatotoxicity. Many plant-derived agents have been accepted to effectively inhibit hepatoma cell invasion. However, the investigation that whether effectual plant-derived agents against invasive hepatoma cells exert unexpected cytotoxicity in healthy hepatocytes has been ignored. This study demonstrated that berberine exhibited significant cytotoxicity in HepG2 cells mainly through upregulation of reactive oxygen species (ROS) production but was ineffective in normal Chang liver cells. Berberine exerted anti-invasive effect on HepG2 cells through suppression of matrix metalloproteinase-9 (MMP-9) expression. Moreover, berberine could significantly inhibit the activity of PI3K-AKT and ERK pathways. Combination treatment of ERK pathway inhibitor PD98059 or AKT pathway inhibitor LY294002 and berberine could result in a synergistic reduction on MMP-9 expression along with an inhibition of cell invasion. Enhancement of ROS production by berberine had no influence on its suppressive effects on the activity of PI3K-AKT and ERK pathways, as well as MMP-9 expression and HepG2 cell invasion. In conclusion, our results suggest that berberine may be a potential alternative against invasive hepatoma cells through PI3K-AKT and ERK pathways-dependent downregulation of MMP-9 expression. This study also provides a previously neglected insight into the investigation of plant-derived agents-based therapy against tumor invasion with the consideration of damage to healthy cells.

A retrospective analysis was done on 43 patients with acute promyelocytic leukemia (APL) at our hospital from June 1987 to August 1992. All-trans retinoic acid was used to induce these patients to differentiation. In the early period of induction there were risks of severe hemorrhage, which was the main cause of early death. Treatments combined with platelets and heparin or aminomethylbenzoic (PAMBA) were given to patients with abnormal coagulation. As a result only 4 out of 43 patients died of intracranial bleeding at 4-12 days when their white blood cell (WBC) counts peaked. The combination of retinoic acid (RA) and HA chemotherapy could reduce hyperleukocytosis during the RA induction course. None of 7 patients died at early stage with this treatment combination. Our studies showed that it could predict the onset of remission at early stage through observations on the successive changes of karyotypes and morphology of the bone marrow and peripheral blood cells. Our studies also showed that the growth of CFU-F could be inhibited by RA. We think that it may play a role in the RA-induced differentiation. In 4 years of follow-up the overall leukemia-free survival (LFS) was 80% with a relapse rate of 45%. Thirty-five patients out of 43 cases were still alive in remission, and one was alive in relapse. All 11 out of 43 patients relapsed within 3 years, but the relapses occurred later, after 3 years duration of remission (P < .01). Retinoic acid failed to induce 5 patients who relapsed with the continuation treatment of RA and chemotherapy alternatively. In order to overcome the resistance to RA, the continuation treatment of simple chemotherapy had been administered following CR. Two cases achieved remission in this way. The difference of resistant events to RA reached significance between these 2 groups of different continuation treatment.

A nonparabolic band model has been implemented for a one-dimensional electron gas, using a modified Schrodinger equation which takes into account size quantization in the transverse cross section of a silicon quantum wire. The quantized states and the corresponding one-dimensional density of states have been analyzed when the nonparabolicity is present, to quantify the importance of the effect of realistic bands at higher energies.