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Chemotherapy regimens that include 5-fluorouracil (5-FU) are central to colorectal cancer treatment; however, risk/benefit concerns limit 5-FU’s use, necessitating development of improved fluoropyrimidine (FP) drugs. In our study, we evaluated a second-generation nanoscale FP polymer, CF10, for improved antitumor activity. CF10 was more potent than the prototype FP polymer F10 and much more potent than 5-FU in multiple colorectal cancer cell lines including HCT-116, LS174T, SW480, and T84D. CF10 displayed improved stability to exonuclease degradation relative to F10 and reduced susceptibility to thymidine antagonism due to extension of the polymer with arabinosyl cytidine. In colorectal cancer cells, CF10 strongly inhibited thymidylate synthase (TS), induced Top1 cleavage complex formation and caused replication stress, while similar concentrations of 5-FU were ineffective. CF10 was well tolerated in vivo and invoked a reduced inflammatory response relative to 5-FU. Blood chemistry parameters in CF10-treated mice were within normal limits. In vivo, CF10 displayed antitumor activity in several colorectal cancer flank tumor models including HCT-116, HT-29, and CT-26. CF10’s antitumor activity was associated with increased plasma levels of FP deoxynucleotide metabolites relative to 5-FU. CF10 significantly reduced tumor growth and improved survival (84.5 days vs. 32 days; P < 0.0001) relative to 5-FU in an orthotopic HCT-116-luc colorectal cancer model that spontaneously metastasized to liver. Improved survival in the orthotopic model correlated with localization of a fluorescent CF10 conjugate to tumor. Together, our preclinical data support an early-phase clinical trial of CF10 for treatment of colorectal cancer.

Chemical looping gasification (CLG) is a recommended method for lignite gasification, and the product syngas is a mixture of H2, CO, and other gases. Much attention has been paid to coal gasification using a fluidized bed for syngas production. In this study, the performance of syngas preparation from CLG using a fluidized bed and CaSO4–CuO as the oxygen carrier was evaluated. To better understand the fluidization process, coal fluidized bed experiments were carried out. Based on the cold-state, syngas obtained from CLG under hot-state conditions was analyzed. The results show that a reaction time of 5 min is recommended for more CO generation. At the same time, a H2/CO molar ratio of around 1 can be achieved. The energy consumption of syngas generation using CaSO4–CuO CLG with lignite is 399.75 kJ mol−1, lower than that of syngas generation using the traditional coal reaction with pure oxygen and steam. This indicates that this is an advanced method for preparing syngas, providing a basis for industrial amplification operations.

Ir catalysts supported on Ce0.9La0.1O2 nanorods and nanoparticles were comparatively investigated for syngas production from methane dry reforming reaction. The exposure of active {110} and {100} crystal planes in the Ir/Ce0.9La0.1O2- nanorods catalysts contributed to the stronger redox property and more oxygen vacancy than those in the Ir/Ce0.9La0.1O2-nanoparticles catalysts. These advantages facilitated activation and transformation of methane and carbon dioxide, giving an enhanced performance of methane dry reforming reaction over the Ir/Ce0.9La0.1O2-nanorods catalysts. The work demonstrated significant influences of support morphologies in obtaining stable catalysts for methane dry reforming reaction.

Non-alcoholic steatohepatitis (NASH) is a severe form of non-alcoholic fatty liver disease characterized by fat accumulation and inflammation in liver. Yet, the mechanistic insight and diagnostic and therapeutic options of NASH remain incompletely understood. This study tested the roles of cysteine protease cathepsin B (CatB) in mouse NASH development. Immunoblot revealed increased liver CatB expression in NASH mice. Fructose-palmitate-cholesterol diet increased body weight gain, liver to body weight ratio, blood fasting glucose, plasma total cholesterol and alanine transaminase levels, and liver triglyceride, but decreased plasma high-density lipoprotein in wild-type mice. All these changes were blunted in CatB-deficient (Ctsb(−/−)) mice. In parallel to reduced expression of genes involved in liver lipid transport and lipogenesis, liver CD36, FABP4, and PPARγ protein levels were also significantly decreased in Ctsb(−/−) mice, although CatB deficiency did not affect liver gluconeogenesis and fatty acid beta-oxidation-associated gene expression. Mechanistic studies showed that CatB deficiency decreased liver expression of adhesion molecules, inflammatory cytokine, and chemokine, along with reduced liver inflammatory cell infiltration. CatB deficiency also promoted M2 macrophage polarization and reduced liver TGF-β1 signaling and fibrosis. Together, CatB deficiency improves liver function in NASH mice by suppressing de novo lipogenesis and liver inflammation and fibrosis.

IgE-mediated activation of Nhe1 (Na + -H + exchanger-1) induces aortic cell extracellular acidification and promotes cell apoptosis. A pH-sensitive probe pHrodo identified acidic regions at positions of macrophage accumulation, IgE expression, and cell apoptosis in human and mouse abdominal aortic aneurysm (AAA) lesions. Ang II (angiotensin II)–induced AAA in Nhe1-insufficient Apoe −/− Nhe1 +/− mice and Apoe −/− Nhe1 +/+ littermates tested Nhe1 activity in experimental AAA, because Nhe1 −/− mice develop ataxia and epileptic-like seizures and die early. Nhe1 insufficiency reduced AAA incidence and size, lesion macrophage and T-cell accumulation, collagen deposition, elastin fragmentation, cell apoptosis, smooth muscle cell loss, and MMP (matrix metalloproteinase) activity. Nhe1 insufficiency also reduced blood pressure and the plasma apoptosis marker TCTP (translationally controlled tumor protein) but did not affect plasma IgE. While pHrodo localized the acidic regions to macrophage clusters, IgE expression, and cell apoptosis in AAA lesions from Apoe −/− Nhe1 +/+ mice, such acidic areas were much smaller in lesions from Apoe −/− Nhe1 +/− mice. Nhe1-FcεR1 colocalization in macrophages from AAA lesions support a role of IgE-mediated Nhe1 activation. Gelatin zymography, immunoblot, and real-time polymerase chain reaction analyses demonstrated that Nhe1 insufficiency reduced the MMP activity, cysteinyl cathepsin expression, IgE-induced apoptosis, and NF-κB activation in macrophages and blocked IgE-induced adhesion molecule expression in endothelial cells. A near-infrared fluorescent probe (LS662) together with fluorescence reflectance imaging of intact aortas showed reduced acidity in AAA lesions from Nhe-1-insufficient mice. This study revealed extracellular acidity at regions rich in macrophages, IgE expression, and cell apoptosis in human and mouse AAA lesions and established a direct role of Nhe1 in AAA pathogenesis.

Synthesis of diethyl carbonate (DEC) in the liquid phase by oxidative carbonylation of ethanol over activated carbon (AC)-supported chloride-free Cu-based catalysts offers a prospective “green chem...

Physiological changes in GTP levels in live cells have never been considered a regulatory step of RAC1 activation because intracellular GTP concentration (determined by chromatography or mass spectrometry) was shown to be substantially higher than the in vitro RAC1 GTP dissociation constant (RAC1-GTP Kd). Here, by combining genetically encoded GTP biosensors and a RAC1 activity biosensor, we demonstrated that GTP levels fluctuating around RAC1-GTP Kd correlated with changes in RAC1 activity in live cells. Furthermore, RAC1 co-localized in protrusions of invading cells with several guanylate metabolism enzymes, including rate-limiting inosine monophosphate dehydrogenase 2 (IMPDH2), which was partially due to direct RAC1-IMPDH2 interaction. Substitution of endogenous IMPDH2 with IMPDH2 mutants incapable of binding RAC1 did not affect total intracellular GTP levels but suppressed RAC1 activity. Targeting IMPDH2 away from the plasma membrane did not alter total intracellular GTP pools but decreased GTP levels in cell protrusions, RAC1 activity, and cell invasion. These data provide a mechanism of regulation of RAC1 activity by local GTP pools in live cells., Changes in intracellular GTP levels are not considered as a regulatory event in RAC1 activation in live cells since total GTP levels are substantially higher than the RAC1 GTP dissociation constant determined in vitro. Here, the authors demonstrate that the availability of free GTP in live cells controls the activity of RAC1 and cell invasion.

NiCuMoLaAl mixed oxide catalysts are prepared and applied in the steam reforming of chloroform-ethyl acetate (CHCl3-EA) mixture to syngas in the present work. The pre-introduction of Cl- ions using chloride salts as modifiers aims to improve the chlorine poisoning resistance. Catalytic tests show that KCl modification is obviously advantageous to increase the catalytic life. The destruction of catalyst structure induced by in situ produced HCl and carbon deposits that occurred on acidic sites are two key points for deactivation of reforming catalysts. The presence of Cl− ions gives rise to the formation of an Ni-Cu alloy, which exhibits a synergetic effect on catalyzing reforming along with metallic Ni crystals formed from excess nickel species, and giving an excellent catalytic stability. Less CHCl3 and more steam can also increase the catalytic stable time of KCl-modified NiCuMoLaAl reforming catalyst.

Developing thermal resistant catalysts is of great interest in heterogeneous catalysis for high temperature catalytic reactions. In this study, embedded Ni catalysts were prepared by co-precipitation method, and were studied for hydrogen production from ethanol steam reforming. The catalysts were characterized by BET, XRD, TEM, H2-TPR and Raman. The results showed that the more Ni embedding and the lower carbon deposits in the 20Ni@CeO2 catalyst exhibited a more stable hydrogen production performance, which should be originated from the more richness of active sites and metal-support interface than that in the 10Ni@CeO2 catalyst, and the more sintering-resistant than that in the 30Ni@CeO2 catalyst. The work provided a potential thermally stable embedded Ni catalyst for stable hydrogen production from ethanol.

Magnetic Ni0.4Co0.2Zn0.4Fe₂O₄ nanoparticles were prepared via the rapid combustion process, the morphology and magnetic property of them were investigated by SEM, TEM, XRD, VSM, and FTIR. The as-prepared magnetic Ni0.4Co0.2Zn0.4Fe₂O₄ nanoparticles calcined at 400 °C for 2 h with absolute alcohol of 20 mL were characterized with the average nanoparticle size of around 25 nm and the specific magnetization of 35.2 emu/g. The adsorption kinetics and adsorption isotherms of Congo red (CR) from aqueous solutions onto Ni0.4Co0.2Zn0.4Fe₂O₄ nanoparticles were investigated by UV spectroscopy at room temperature; the adsorption kinetics data were in good agreement with the pseudo-second-order kinetic model in the initial CR concentrations of 200-500 mg/L. By comparison of Langmuir, Freundlich and Temkin models for adsorption isotherms of CR, the Temkin model (correlation coefficient R₂ = 0.9969) could be used to evaluate the adsorption isotherm of CR onto the magnetic Ni0.4Co0.2Zn0.4Fe₂O₄ nanoparticles at room temperature, which suggested that the adsorption of CR onto the magnetic Ni0.4Co0.2Zn0.4Fe₂O₄ nanoparticles was a hybrid of monolayer and multilayer absorbing mechanism.

Mast cell (MC) deficiency in KitW-sh/W-sh mice and inhibition with disodium chromoglycate (DSCG) or ketotifen reduced obesity and diabetes in mice on a high-cholesterol (1.25%) Western diet. Yet, Kit-independent MC-deficient mice and mice treated with DSCG disproved MC function in obesity and diabetes when mice are fed a high-fat diet (HFD) that contains no cholesterol. This study reproduced the obesity and diabetes inhibitory activities of DSCG and ketotifen from mice on a Western diet. Yet, such inhibitory effects were diminished in mice on the HFD. DSCG and ketotifen MC inhibitory activities were recovered from mice on the HFD supplemented with the same amount of cholesterol (1.25%) as that in the Western diet. DSCG and ketotifen effectively blunted the high-cholesterol diet-induced elevations of blood histamine and adipose tissue MC degranulation. Pearson's correlation test demonstrated significant and positive correlations between plasma histamine and total cholesterol or low-density lipoprotein-cholesterol (LDL). In cultured bone marrow-derived MCs, plasma from mice following a Western diet or a cholesterol-supplemented HFD, but not those from HFD-fed mice, induced MC degranulation and the release of β-hexosaminidase, histamine, and serotonin. IgE, LDL, very low-density lipoprotein, and high-density lipoprotein also induced MC activation, which can be inhibited by DSCG and ketotifen depending on the doses and types of MC inhibitors and cholesterol, and also the MC granule molecules of interest. DSCG or ketotifen lost their activities in inhibiting LDL-induced activation of MCs from LDL receptor-deficient mice. These results indicate that dietary cholesterol critically influences the function of mouse MCs.

Background Our aim was to explore the potential mechanism underlying papillary thyroid carcinoma (PTC) development. Methods Gene expression profile data GSE3467 and microRNA (miRNA) expression profile data E-TABM-68 were downloaded from Gene Expression Omnibus and Array Express database respectively. The differentially expressed genes (DEGs) and miRNAs between PTC patients and normal individuals were screened. Then, the significant target DEGs regulated by differentially expressed miRNAs were mapped to protein-protein interaction (PPI) network and functional modules were screened. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis for miRNA genes were performed using DAVID (the Database for Annotation, Visualization and Integration Discovery) tool. Results Total 4307 DEGs and 23 differentially expressed miRNAs were identified. A PPI subnetwork containing 612 nodes and 713 edges was constructed. Total 5 DEGs such as SPARC (secreted protein acidic and rich in cysteine), FN1 (fibronectin 1), THBS1 (thrombospondin 1), COL1A1 (collagen, type I, alpha 1) and COL7A1 (collagen, type VII, alpha 1) were found in module M1. The up-regulated DEGs were significantly related with cell adhesion molecules (CAMs), response to wounding and immune response. The down-regulated DEGs were significantly enriched in metabolism related pathways and transcription related with GO terms. Conclusions ECM-receptor interaction and amino acid degradation may play key roles in the mechanism of PTC progression.

M2-like tumour-associated macrophages (TAMs) have been demonstrated to promote the growth of anaplastic thyroid carcinoma (ATC). However, the underlying mechanism of M2-like TAMs in ATC remains unclear. Thus, in the present study, the role and mechanism of M2-like TAMs in ATC were investigated. M2-like TAMs were induced by treatment with PMA, plus IL-4 and IL-13, and identified by flow cytometry. Transwell and sphere formation assays were applied to assess the invasion and stemness of ATC cells. The expression levels of insulin-like growth factor (IGF)-1 and IGF-2 were examined by ELISA and reverse transcription-quantitative PCR. Proteins related to the epithelial-mesenchymal transition (EMT), stemness and the PI3K/AKT/mTOR pathway were examined via western blotting. Immunohistochemistry (IHC) was used to detect the expression of the M2-like TAM markers CD68 and CD206 in ATC tissues and thyroid adenoma tissues. It was found that treatment with PMA plus IL-4 and IL-13 successfully induced M2-like TAMs. Following co-culture with M2-like TAMs, the invasive ability and stemness of ATC cells were significantly increased. The expression levels of the EMT-related markers N-cadherin and Vimentin, the stemness-related markers Oct4, Sox2 and CD133, and the insulin receptor (IR)-A/IGF1 receptor (IGF1R) were markedly upregulated, whereas E-cadherin expression was significantly decreased. In addition, the production of IGF-1 and IGF-2 was significantly increased. Of note, exogenous IGF-1/IGF-2 promoted the invasion and stemness of C643 cells, whereas blocking IGF-1 and IGF-2 inhibited metastasis and stemness by repressing IR-A/IGF-1R-mediated PI3K/AKT/mTOR signalling in the co-culture system. IHC results showed that the expression of CD68 and CD206 was obviously increased in ATC tissues. To conclude, M2-like TAMs accelerated the metastasis and increased the stemness of ATC cells, and the underlying mechanism may be related to the section of IGF by M2-like TAMs, which activates the IR-A/IGF1R-mediated PI3K/AKT/mTOR signalling pathway.

Aims This study aims to explore the effect and underlying mechanism of zoledronic acid (ZA) on the incidence of thyroid cancer (TC) tumorigenesis. Materials and methods Human mononuclear cells THP-1 were differentiated into M2-like tumor associated macrophages (TAMs) by incubation with PMA followed by additional incubation of IL-4 and IL-13. TC cells TPC-1 and IHH4 were co-cultured with M2-like TAMs. Identification of M2-like TAMs markers were determined by immunohistochemistry or flow cytometry. Cell proliferation, stemness and migration/invasion ability were measured by colony, sphere formation assay and transwell assay, respectively. The expression levels of cell stemness, EMT and Wnt/β-catenin pathway-related factors were verified by qRT-PCR, Western blotting, and immunofluorescence. A subcutaneous tumor model was established in nude mice to examine the in vivo effects of ZA. Key findings M2-like TAMs were enriched in TC tissues, and they promoted the colony/sphere formation, accompanied with a down-regulated expression in E-cadherin and an up-regulated expression in N-cadherin, Vimentin and other stemness-associated markers (CD133, Oct4, c-Myc) in TC cells. The effects were suppressed when ZA co-treatment was given, because ZA inhibited the polarization of M2-like TAMs and β-catenin entry into the nucleus. Moreover, in agreement with in vitro data, ZA also limited subcutaneous tumor formation and macrophage enrichment in nude mice. Significance ZA suppressed M2-like TAMs induced TC cell proliferation, stemness and metastasis through inhibiting M2-like TAMs polarization and Wnt/β-catenin pathway, which sheds light on the mechanisms of TC and provides avenues for the development of clinical therapy to TC.

Objective: By binding to its high-affinity receptor FcεR1, IgE activates mast cells, macrophages, and other inflammatory and vascular cells. Recent studies support an essential role of IgE in cardiometabolic diseases. Plasma IgE level is an independent predictor of human coronary heart disease. Yet, a direct role of IgE and its mechanisms in cardiometabolic diseases remain incompletely understood. Approach and Results: Using atherosclerosis prone Apoe −/− mice and IgE-deficient Ige −/− mice, we demonstrated that IgE deficiency reduced atherosclerosis lesion burden, lesion lipid deposition, smooth muscle cell and endothelial cell contents, chemokine MCP (monocyte chemoattractant protein)-1 expression and macrophage accumulation. IgE deficiency also reduced bodyweight gain and increased glucose and insulin sensitivities with significantly reduced plasma cholesterol, triglyceride, insulin, and inflammatory cytokines and chemokines, including IL (interleukin)-6, IFN (interferon)-γ, and MCP-1. From atherosclerotic lesions and peritoneal macrophages from Apoe −/− Ige −/− mice that consumed an atherogenic diet, we detected reduced expression of M1 macrophage markers (CD68, MCP-1, TNF [tumor necrosis factor]-α, IL-6, and iNOS [inducible nitric oxide synthase]) but increased expression of M2 macrophage markers (Arg [arginase]-1 and IL-10) and macrophage-sterol-responsive-network molecules (complement C3, lipoprotein lipase, LDLR [low-density lipoprotein receptor]-related protein 1, and TFR [transferrin]) that suppress macrophage foam cell formation. These IgE activities can be reproduced in bone marrow-derived macrophages from wild-type mice, but muted in cells from FcεR1-deficient mice, or blocked by anti-IgE antibody or complement C3 deficiency. Conclusions: IgE deficiency protects mice from diet-induced atherosclerosis, obesity, glucose tolerance, and insulin resistance by regulating macrophage polarization, macrophage-sterol-responsive-network gene expression, and foam cell formation.

Backgrounds. Doxorubicin (DOX) is an effective therapeutic drug for malignant tumors; however, its clinical applications were limited by its side effects, especially the cardiotoxicity caused by ROS-mediated p53 and MAPK signal pathways’ activation-induced cell apoptosis. Sanyang Xuedai mixture (SYKT) has been reported as an antioxidant agent and attenuated DOX-induced cardiotoxicity by targeting ROS-mediated apoptosis, but the mechanisms are still not fully delineated. Objective. This study aimed at investigating whether SYKT alleviated DOX-induced cardiotoxicity by inhibiting ROS-mediated apoptosis and elucidating the role of ROS-mediated p53 and MAPK signal pathways’ activation in this process. Materials and Methods. Identification, separation, and culture of mouse primary cardiomyocytes. Cells were treated with DOX (1 μM), SYKT (30 mg/mL), or SYKT coupled with DOX. The p53 inhibitor Pifithrin-α (PFT-α), p38/MAPK inhibitor SB203583 (SB), and JNK inhibitor SP600125 (SP) were used as positive control. Western blot was employed to detected p53 and p38 as well as JNK expressions and the activation and translocation of Bax and cytochrome C. Flow cytometer (FCM) was used to detect the mitochondrial membrane potential and cell apoptosis. Results. After separation and culture, 95% of cells showed positive cTnI expression, which indicated that mouse primary cardiomyocytes were successfully identified in our research. DOX activated p53 and MAPK signal pathways in a time-dependent manner, which were inactivated by being cotreated with SYKT, PFT-α, or SB, respectively. DOX significantly decreased Bax and increased cytochrome c expressions in the cytoplasm, whereas Bax was upregulated and cytochrome c was downregulated in the mitochondria, which were reversed by SYKT treatment. Besides, DOX reduced mitochondria membrane potential (MMP) in cardiomyocytes compared to the control group; SYKT recovered its MMP and attenuated DOX-induced cardiomyocyte injury. Of note, DOX increased the expression levels of cleaved caspase-3 as well as poly ADP-ribose polymerase (PARP) and promoted cell apoptosis, which were also reversed by SYKT treatment. Discussion and Conclusions. Our results indicated that SYKT alleviated DOX-induced cardiotoxicity by inhibiting p53 and MAPK signal pathways’ activation-mediated apoptosis, and it might serve as a potential therapeutic agent for DOX-induced cardiotoxicity.

Structure stability of CeO2 nanoparticles and nanorods were studied for ethanol steam reforming reaction over Ir/CeO2 nanocatalysts. Characterizations of BET, XRD, HRTEM, H2-TPR and H2O-TPD et al. were applied to analyze surface areas, sizes, morphologies, redox properties and water activation of the nanocatalysts. Performance results revealed that reaction patterns of ethanol steam reforming reaction were dependent on the structures of CeO2 supports, originating from different abilities in water activation. After long time stability tests conducted at high temperature of 923 K, the CeO2 nanoparticles maintained original polyhedral shape, while the CeO2 nanorods changed to polyhedrons. The shape variation of the nanorods was supposed to associated with OH groups combination and oxygen exchange in surface crystal planes of ceria nanorods, which diminished oxygen vacancies and reconstructed ceria morphology.

In this study, we aimed at investigating effects of lncRNA ADAMTS9-AS2 on lung cancer progression through regulating miR-223-3p and TGFBR3 expressions. Expressions of ADAMTS9-AS2 in lung cancer tissues and cell lines were determined by reverse transcriptase polymerase chain reaction (qRT-PCR). TargetScan and miRcode were used to predict the targeting relationships, respectively. The luciferase reporter system was used to verify that the relationship among ADAMTS9-AS2, TGFBR3 and miR-223-3p. Western blot assay tested the protein level changes in TGFBR3. Cell proliferation was determined by CCK-8 assay. Cell cycle and cell apoptosis were detected by flow cytometry assay, and migration and invasion were determined by transwell assay. Tumor xenograft model was developed to study the influence of ADAMTS9-AS2 on tumor growth in vivo. qRT-PCR results demonstrated that lncADAMTS9-AS2 was lowly expressed in lung cancer tissues. High expression of ADAMTS9-AS2 in lung cancer cells significantly reduced proliferation ability and inhibited migration, as well as elevating their apoptosis rate. In vivo assay found that ADAMTS9-AS2 suppressed the lung tumor growth. Bioinformatics predicted that miR-223-3p bound directly to the ADAMTS9-AS2 and TGFBR3, which was later confirmed by luciferase reporter system. ADAMTS9-AS2 transfection increased TGFBR3 mRNA and protein expressions in lung cancer cells, but miR-223-3p transfection significantly decreased them. Besides, our results showed that miR-223-3p induced cellular apoptosis while TGFBR3 group showed the complete opposite effect. It was proved that ADAMTS9-AS2 and TGFBR3 were the direct genes of miR-223-3p. MiR-223-3p promotes proliferation, migration and invasion of lung cancer cells by targeting TGFBR3. Therefore, ADAMTS9-AS2, miR-223-3p and TGFBR3 may provide potential targets for the treatment of lung cancer patients. © 2018 IUBMB Life, 70(6):536-546, 2018.

Thyroid carcinoma is primarily treated by surgery combined with radioactive 131iodine (131I) treatment; however, certain patients exhibit resistance to 131I treatment. Previous research indicated that nuclear factor-κB (NF-κB) was associated with resistance to 131I in cancer cells. The present study aimed to investigate the effects of NF-κB on 131I uptake and apoptosis in thyroid carcinoma cells. TPC-1 and BCPAP cell lines were employed as research models in the present study, and the expression of NF-κB was inhibited by RNA interference (RNAi). The ability of TPC-1 and BCPAP cells to uptake 131I was measured and the cell viability was detected by an MTT assay. Finally, the expression of the apoptosis-associated proteins X-linked inhibitor of apoptosis (XIAP), cellular inhibitor of apoptosis protein 1 (cIAP1) and caspase-3 in TCP-1 and BCPAP cells was determined by western blotting. Western blotting results demonstrated that the expression levels of NF-κB in TPC-1 and BCPAP cells were successfully downregulated by RNAi (P0.05). MTT experiments demonstrated that the inhibition of NF-κB expression in combination with radiation (131I treatment) led to a marked reduction in cell viability (P

In this study, potassium persulfate, N,N'-methylene bisacrylamide (MBA), and soluble starch (ST) were in situ cross-linked into porous antimicrobial starch particles containing N-halamine functional groups (PST–MBA–Cl). Then, polyacrylonitrile (PAN)/silica aerogel (SA)/zinc oxide (ZnO) beaded fibers containing PST–MBA–Cl particles were prepared by electrospinning. Scanning electron microscopy results demonstrated the uniform dispersion of the PST–MBA–Cl particles and ZnO on the surface and interior of the beaded fiber when the concentration of the PST–MBA–Cl particles was 15%. The composite beaded fibers prepared after chlorination and soaking in zinc salt solutions of different pH values had a higher degree of interior fluffiness. For the analysis of the effectivity of the prepared particles using 108 CFU/mL gram-positive (S. aureus) and gram-negative (E. coli) bacterial human pathogens, the inhibition zone was 15.97 ± 0.12 and 17.81 ± 0.23 mm, respectively. Meanwhile, the degradation efficiency of PAN and SA for the cationic dye methylene blue (MB) was 88.00% ± 1.83%. The PAN/SA/PST–MBA–Cl/ZnO composite beaded fiber showed good antibacterial properties and a fast recovery rate, and its degradation efficiency for MB was retained at ~80% after five cycles. Thus, the PAN/SA/ PST–MBA–Cl/ZnO beaded fibers can be used as an environment-friendly and reusable adsorbing material for the removal of dyes from industrial wastewater.

Thermal catalysis is the most investigated approach for methane dry reforming (MDR) reaction over Ni-based catalysts. However, sintering and carbon deposition in the conventional approach tend to deactivate the Ni catalysts. Developing new technique to resolve the problems is a hot topic for MDR. Herein, we reported a novel (Ni/CeO2)@SiO2 catalyst for MDR by photothermal catalysis. The catalyst was characterized by BET, XRD, TEM and UV–vis diffuse reflectance spectrum to analysis structural and optical properties, which were applied to build relationship with MDR performance. The results revealed that band gap energy of ceria in the catalyst was significantly narrowed by the tiny size of crystal ceria, leading to strong absorbance of visible solar light. The adsorption considerably promoted activations of CH4 on Ni and CO2 on CeO2, and greatly improved gasification of CHx at Ni-CeO2 boundaries. Along with confinement effect from silica shell, sintering and carbon deposition were both resolved for the (Ni/CeO2)@SiO2 catalyst in photothermal MDR. Consequently, photothermal MDR was higher and more stable than thermal MDR over the catalyst. The work provided a new way of photothermal MDR to enhance activity and stability, and simultaneously resolved problems of sintering and carbon deposition.

A series of Ce 0.90 Co 0.10 O 2 − δ and Ce 0.90 − x Cu x Co 0.10 O 2 − δ (x = 0.03, 0.07 and 0.10) catalysts synthesized by an alkaline hydrothermal method were utilized as ozonation catalysts for the NO X (x = 1, 2) removal at low temperatures. A novel catalyst-duct separation apparatus for denitrification by catalytic ozonation was developed by our group. Ce 0.83 Cu 0.07 Co 0.10 O 2 − δ exhibits the highest catalytic activity (91.5% removal at 120 °C), whereas Ce 0.80 Cu 0.10 Co 0.10 O 2 − δ presents the lowest (74.1% removal at 120 °C). Only NO 3 − is detected in the tail solutions. The catalytic performance presents a positive relationship with the corresponding OH concentration. OH radical can be “transferred” from catalyst surface to the duct, prolonging activation time through its own reproduction reaction. The surface –OH activation, not the surface –OH density determines the OH concentration in the present method. Ce 0.83 Cu 0.07 Co 0.10 O 2 − δ contains a large number of high-activation bridging –OH, whereas the bridging –OH is absent in Ce 0.80 Cu 0.10 Co 0.10 O 2 − δ . Therefore, Ce 0.83 Cu 0.07 Co 0.10 O 2 − δ shows much higher activation for promoting the formation of OH than Ce 0.80 Cu 0.10 Co 0.10 O 2 − δ .

Co 3 O 4 nanomaterials were synthesized by hydrothermal method and were applied for low temperature CO oxidation and methane combustion. The addition of ethylene glycol and its concentration significantly influenced the size and shape of the Co 3 O 4 oxides. Nanosheets of Co 3 O 4 were synthesized in ethylene glycol solution and nanospheres were formed in water. The activity of oxygen species in the nanosheets and nanospheres were characterized by hydrogen/methane programmed reduction, oxygen programmed desorption and XPS. The results showed that the Co 3 O 4 nanosheets exhibited more active oxygen species than the Co 3 O 4 nanospheres, leading to the higher activity in the oxidative reactions. The study demonstrated the importance of active oxygen species in Co 3 O 4 catalysts to achieve high catalytic performance towards the carbon monoxide and methane elimination at low temperatures.

Regulatory T cells (Tregs) play essential roles in obesity and diabetes. Here, we report a role of Tregs in enhancing β3-adrenergic receptor agonist CL316243 (CL)-stimulated thermogenic program in subcutaneous adipose tissue (SAT), but not in visceral fat. CL treatment for 7 days increased SAT adipocyte beiging and thermogenic gene expression in male or female mice. Adoptive transfer of Tregs enhanced this CL activity. Such Treg activity lost in male epididymal white adipose tissue (eWAT) and female gonadal gWAT. Adipocyte culture yielded the same conclusion. Tregs enhanced the expression of CL-induced thermogenic genes in SAT from male and female mice. This activity of Tregs reduced or disappeared in adipocytes from eWAT or gWAT. Both CL and Tregs induced much higher UCP-1 (uncoupling protein-1) expression in SAT from females than that from males. A mechanistic study demonstrated a role of Tregs in suppressing the expression of M1 macrophage markers (Tnfa, Il6, iNos, Ip10) and promoting the expression of M2 macrophage markers (Mrc1, Arg1, Il10) in bone-marrow-derived macrophages or in SAT from male or female mice. In female mice with pre-established obesity, Treg adoptive transfer reduced the gWAT weight in 2 weeks. Together with CL treatment, Treg adoptive transfer reduced the SAT weight and further improved CL-induced glucose metabolism and insulin sensitivity in female obese mice, but did not affect CL-induced body weight loss in male or female obese mice. This study revealed a predominant role of Tregs in female mice in promoting adipocyte beiging and thermogenesis in SAT, in part by slanting M2 macrophage polarization.

Low temperature methane dry reforming by Ni-based catalysts is an economic way to convert greenhouse gases of CH4 and CO2, but carbon deposition is a great challenge. Taking the advantage of mobile oxygen on CeO2, we synthesized a Ni@SiO2@CeO2 catalyst by coating ceria on surface of Ni@SiO2 to reduce carbon deposition. H2 temperature-programmed reduction, X-ray photoelectron spectra and oxygen temperature-programmed desorption demonstrated the high oxygen mobility from ceria in Ni@SiO2@CeO2 catalyst, which significantly reduced carbon deposition and enhanced stability of methane dry reforming reaction. Experimental results revealed that methane dry reforming performance was one and a half times higher, but carbon deposition was one half lower, over the Ni@SiO2@CeO2 catalyst than over the Ni@SiO2 catalyst. The strategy of ceria coating in reducing carbon deposition and enhancing reaction stability could also be applied to other heterogeneous reactions suffering carbon deposition.

Radioresistance is a crucial factor for the failure of iodine 131 (131I)-based radiotherapy for differentiated thyroid carcinoma (DTC). This study aimed to explore the effect of circ_NEK6 on the development of 131I resistance in DTC and its potential mechanism. In this study, we demonstrated that circ_NEK6 expression was significantly elevated in 131I-resistant DTC tissues and cell lines. Knockdown of circ_NEK6 significantly repressed 131I resistance via inhibiting cell proliferation, migration, invasion abilities, and inducing cell apoptosis and DNA damage in 131I-resistant DTC cells. Mechanistically, knockdown of circ_NEK6 suppressed 131I resistance in DTC by upregulating the inhibitory effect of miR-370-3p on the expression of myosin heavy chain 9 (MYH9). In vivo experiments showed that circ_NEK6 inhibition aggravated 131I radiation-induced inhibition of xenograft tumor growth. Taken together, knockdown of circ_NEK6 repressed 131I resistance in DTC cells by regulating the miR-370-3p/MYH9 axis, indicating that circ_NEK6 may act as a potential biomarker and therapeutic target for DTC patients with 131I resistance.

In this paper, copper ferrite(CuFe2O4), prepared by a hydrothermal method, was successfully utilized in catalytic ozonation for NOx removal. CuFe2O4 shows higher activity (83%) than both CuO (79%) and Fe2O3 (70%). Hydroxyl radicals (OH) have been detected in the catalytic ozonation process, which has been confirmed to determine the catalytic performance of NOx removal. Compared to CuO and Fe2O3, CuFe2O4 exhibits more surface hydroxyl groups and oxygen vacancies, indicating that the synergetic effect of the surface hydroxyl groups and oxygen vacancies plays an important role in the enhancement of the generation of hydroxyl radicals, thus the catalytic activity. A possible mechanism for the catalytic ozonation of NOx was proposed.

Nanostructured F doped cerium and titanium mixed oxide catalyst (CeTiF) and cerium and titanium mixed oxide catalyst (CeTi) were prepared by co-precipitation method. The F is for the first time to be doped into CeTi as the ozonation catalyst. Compared to CeTi, the catalyst of CeTiF exhibited a better catalytic activity, yielding 83% NOx (x = 1, 2) conversion at 40 °C. In order to investigate the effect of F on CeO2-TiO2 catalysts for the catalytic ozonation of NOx (x = 1, 2), the catalysts were characterized by XRD, PL spectra, Raman spectra, XPS, TGA, NH3-TPD and FTIR techniques. The CeTiF exhibits higher catalytic activity than CeTi, which is found that it presents linear relationship with the OH radical concentration. The doping of F does substitute the O in Ce O Ti, Ti O Ti or Ce O Ce linkage bonds to produce more oxygen vacancies, and slightly enhances the BET surface area and hydrophilicity, which promote the chemisorption of H2O to form surface OH, and benefiting the O3 adsorption on the surface OH, thus promoting the production of OH, further improving the catalytic performance. These oxygen vacancy and surface hydroxyl groups play a critical role in the OH production for NOx removal.

Water plays a crucial role in the synthesis mechanism of metal organic framework-5 (MOF-5). Synthesized MOF-5 with good phase structure and large specific surface area is largely determined by an important synthesis factor: the total water concentration of the initial synthesis solution (C tw ). An understanding of the effects of different and high C tw on the synthesis of MOF-5 and the investigation of the maximum C tw suitable for the synthesis of MOF-5 are important to guide the synthesis of MOF-5. Through the research of the maximum C tw , a favorable synthetic approach was established which could realize the synthesis of MOF-5 with fine performance on CO2 adsorption and separation. The research results show that the maximum C tw could be as high as 1,440mmol/L, and synthesized MOF-5 still has a good phase structure and a large specific surface area of 2,136m2/g (BET). Synthesized MOF-5 by the maximum C tw exhibits a high CO2 adsorption capacity of 2.5mmol/g and a low N2 adsorption capacity of 0.2mmol/g at 298 K and 100 kPa. More importantly, synthesized MOF-5 by the maximum C tw exhibits a high selectivity for CO2/N2 of 18-22 at 298 K and 20-130 kPa in simulated flue gas.

In this paper, CO atmosphere reduced cobalt manganate (CoMn2O4/CO), prepared by a hydrothermal method, was successfully utilized in catalytic ozonation for NOx removal. CoMn2O4/CO shows higher activity (84%) than CoMn2O4/air (82%), Co3O4 (76%) and Mn2O3 (76%). Hydroxyl radicals (·OH) have been detected in the catalytic ozonation process, which has been confirmed to determine the catalytic performance of NOx removal. Compared to Co3O4 and Mn2O3, CoMn2O4 exhibits more surface hydroxyl groups and oxygen vacancies, both of which are critical for the ·OH generation. More importantly, more oxygen vacancies are generated when the CoMn2O4 is calcined in the reduced atmosphere. These oxygen vacancies benefit the adsorption of sufficient H2O to yield active surface –OH on the catalyst surface, promoting the adsorption of O3 on the surface –OH and thus the production of ·OH radicals. A possible mechanism for the catalytic ozonation of NOx was proposed.

CeO2 grown on a reduced graphene oxide nanocomposite (RGO–CeO2) was successfully synthesized by a facile alkaline hydrothermal method with the addition of ethylene glycol. For the first time, it was utilized as an ozonation catalyst for denitrification at low temperatures. The RGO–CeO2 nanocomposite, in which the content of RGO was only 2.8 wt%, exhibited much higher catalytic activities (96.8% at 40 °C) than pure nano-CeO2 (78.2% at 40 °C), which was found to exhibit a positive relationship with the concentration of ˙OH radicals. There was no correlation between the surface hydroxyl densities and the catalytic activities of RGO–CeO2, RGO and CeO2, suggesting that not all surface hydroxyl groups exhibit the same high catalytic activity. The activity of surface hydroxyl groups becomes the dominant factor for determining catalytic performance. Compared with pure nano-CeO2, the surface hydroxyl activity was enhanced for RGO–CeO2 due to the generation of more oxygen vacancies from the reduction in crystallite size and better dispersion of CeO2. The surface –OH groups at the oxygen vacancy sites were more active than the intrinsic –OH of CeO2 at promoting the generation of ˙OH radicals and being conducive to denitrification.

A vast amount of evidence indicates that long non-coding RNAs (lncRNAs) are involved in cancer. Previous studies have indicated that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) is aberrantly expressed in lung cancer, pancreatic ductal adenocarcinoma and hepatocellular carcinoma. However, the role of DGCR5 in papillary thyroid carcinoma (PTC) has remained elusive. In the present study, it was revealed that DGCR5 was significantly downregulated in PTC tissues compared with that in adjacent normal tissues. Through functional experiments, it was demonstrated that ectopic overexpression of DGCR5 markedly suppressed PTC cell growth and invasion. A bioinformatics analysis suggested that DGCR5 binds to microRNA (miR)-2861. A total of 5 putative binding sites for miR-2861 were identified in DGCR5, and a luciferase reporter assay confirmed the direct interaction between DGCR5 and miR-2861. Furthermore, reverse transcription-quantitative polymerase chain reaction analysis indicated that ectopic overexpression of DGCR5 led to a decreased expression of miR-2861 in PTC cells and miR-2861 mimic transfection caused a downregulation of DGCR5. miR-2861 level was upregulated in PTC tissues compared with adjacent tissues and negatively correlated with DGCR5 level. In addition, rescue experiments indicated that ectopic expression of miR-2861 reversed the effects of DGCR5 overexpression on PTC cell proliferation and invasion. Taken together, the present results demonstrated that DGCR5 inhibits PTC progression via sponging miR-2861, indicating DGCR5 may serve as a therapeutic target.

Ginsenoside-Rg1 (G-Rg1) is an agent isolated from Panax ginseng that exerts anti-fibrotic effects; however, the mechanism is still unclear. Herein, we investigated whether G-Rg1 administration can mitigate or reverse unilateral ureteral obstruction (UUO)-induced renal fibrosis by regulating the Klotho/transforming growth factor (TGF)-β1/Smad signaling pathway in rats. Sprague-Dawley male rats were subjected to UUO, and rats in the treatment group were administered G-Rg1 or G-Rg1 plus Klotho short hairpin RNA interference (shRNA), while rats in the control and model groups were administered vehicle for 14 d. Epithelial-mesenchymal transition (EMT) biomarkers and Klotho/TGF-β1 signaling molecules were examined by immunohistochemistry, quantitative real-time PCR and Western blotting. Immunohistochemistry showed that UUO induced increased pro-fibrotic TGF-β1 expression, overexpression of the mesenchymal marker, α-smooth muscle actin (α-SMA), and suppression of the epithelial marker, E-cadherin. Moreover, Western blotting analysis indicated that UUO promoted TGF-β1 and phosphorylated Smad3 (p-Smad3) expression (p

Objectives The intention of our study was to investigate the relationship between miR‐144‐3p and EZH2 as well as the effects of their interaction on cell propagation and invasiveness in lung adenocarcinoma (LUAD). Methods The expression levels of miR‐144‐3p and EZH2 in LUAD tissues and normal tissues were determined by qRT‐PCR. The dual‐luciferase reporter assay was utilized to validate the targeting relationship between miR‐144‐3p and EZH2. MTT assay and colony formation assay were performed to evaluate the viability and propagation of LUAD cells, while the effects of miR‐144‐3p and EZH2 on LUAD cell invasiveness were confirmed by transwell assay. Protein expression levels of VEGFA, MMP2, and MMP9 were measured by Western blot. Furthermore, xenograft tumor models were established to verify the effects of miR‐144‐3p on tumor formation and EZH2, VEGFA, MMP2 and MMP9 expressions in vivo. Results miR‐144‐3P was downregulated in LUAD tissues, and overexpression of miR‐144‐3p inhibited propagation and invasiveness of LUAD cells. EZH2 was a target of miR‐144‐3p and was highly expressed in LUAD cells. Knockdown of EZH2 could suppress the propagation and invasion of LUAD cells. Increased miR‐144‐3p expression exerted an inhibitory effect on LUAD tumor formation in vivo. Conclusion Overexpression of miR‐144‐3p impeded the propagation and invasiveness of LUAD cells by targeting EZH2.

Multidrug resistance (MDR) is an obstacle for cancer chemotherapy. It was reported that 20(S)-ginsenoside Rg3 (hereafter Rg3) was able to regulate MDR in mouse leukemia cells. The present study investigated the effect of Rg3 on the MDR of A549 lung cancer cells. A cell viability assay revealed that Rg3 treatment increased cisplatin (DDP) cytotoxicity in DDP resistant A549 cells (A549/DDP). Furthermore, Rg3 increases the antitumor effect of DDP on A549/DDP xenograft mice. The expression of MDR-mediated proteins, including P-glycoprotein (P-gp), multidrug resistance-associated protein (MPR1) and lung resistance protein 1 (LPR1), was detected in tumor tissue of A549/DDP xenograft mice. The results revealed that Rg3 treatment inhibited the expression of these MDR-associated proteins. Additionally, technetium-99m labeled hexakis-2-methoxyisobutylisonitrile (99mTc-MIBI) single-photon emission computed tomography was used to monitor the effect of Rg3 on cisplatin sensitivity of A549/DDP xenograft tumors. It was observed that uptake of 99mTc-MIBI was increased by Rg3 treatment, which indicated that Rg3 is able to effectively enhance chemotherapy sensitivity of A549/DDP xenograft tumors. Taken together, these results revealed that Rg3 may be able to reverse MDR of lung cancer via the downregulation of P-gp, MPR1 and LPR1.

The kinetic behavior of preparing diphenyl carbonate by the transesterification of dimethyl carbonate with phenol in a reactive distillation reactor has been explored experimentally and theoretically. The transesterification reaction was described to conform a pseudo-second-order kinetics, and a semi-empirical kinetic model has been derived to explain the kinetic behavior. The model parameters were fitted to experimental data by an improved genetic algorithm. The proposed model was determined to be useful in simulating the rate constant and the mole fraction of components, which agreed well with the experimental data for different operating temperatures and catalyst concentrations.

MoO3/SiO2 catalysts for the transesterification of dimethyl oxalate (DMO) with phenol were prepared by both the thermal spreading (TS) and incipient wetness impregnation methods. The results showed that the 10%MoO3/SiO2 catalyst prepared by TS (10%MoO3/SiO2-TS) exhibited higher catalytic performance compared with the 10%MoO3/SiO2 catalyst prepared by incipient wetness impregnation (10%MoO3/SiO2-C). The catalysts were characterized by X-ray diffraction, Raman spectroscopy, X-ray photoelectron spectroscopy, pyridine-IR spectroscopy, and NH3 temperature- programmed desorption. These analyses indicated that weak Lewis acid sites were formed on the catalyst surfaces and that the Mo species were present as monomeric MoO3 rather than as isolated molybdenum oxide or polymolybdate species on both catalysts, although the 10%MoO3/SiO2-TS exhibited better dispersion of MoO3 and a higher surface Mo content than the 10%MoO3/SiO2-C. Under the optimal transesterification reaction conditions (1.2 g 10%MoO3/SiO2-TS, T = 180 °C, n(DMO)/n(phenol) = 2, t = 4 h), the conversion of phenol was 70.9%, and the yields of methyl phenyl oxalate and diphenyl oxalate were 63.1% and 7.7%, respectively.

Dimethoxymethane was first synthesized from methanol with a liquid phase intermittent process which only used molecular oxygen as the sole oxidant. RuCl3 was proved to be an efficient catalyst as it posses the ability of oxidizing methanol and Lewis acidic which promotes the oxidation of methanol to formaldehyde and then methanol condensed with formaldehyde to form dimethoxymethane at Lewis acid site.

During the process of curve section or long radius drilling in the horizontal well, between the drilling string and wellbore, the phenomenon of friction, sticking and backing pressure is very serious. The newly developed Hydro-oscillator could make vibration in radial direction and axial ones. So the tool could reduce the sliding friction and increase the effective drilling weight of the bit(WOB). This tool was widely tested in Changqing oilfield. The result shows that the sliding drilling speed is up to 100.96% and sliding drilling achieved significant results with this tool.

Background: Our previous studies have demonstrated that hepatic expression of apolipoprotein A-IV (apoA-IV) is increased in mouse models of chronic steatosis and is closely correlated with hepatic triglyceride (TG) content. We have also shown that steatosis-induced hepatic apoA-IV gene expression is regulated by processing of the nuclear transcription factor cAMP responsive element-binding protein H (CREBH). Herein, we explored the mechanisms that mediate steatosis-induced CREBH processing. Methods: We measured hepatic CREBH processing, apoA-IV gene expression, and lipid content in several mouse models of attenuated or enhanced VLDL assembly that were subjected to acute steatosis induced by a 16 hour overnight fast or by feeding a ketogenic diet for 6 days. Results: Both fasting and the ketogenic diet induced acute hepatic TG accumulation associated with increased CREBH processing and apoA-IV gene expression, which were associated with hepatic TG content in C57BL/6 mice. All mouse models of attenuated VLDL secretion (shRNA-induced apoB knock down, liver specific microsomal triglyceride transfer protein (MTP) knockout, treatment with the MTP inhibitor BMS212122, and comparative gene identification-58 (CGI-58) deficiency) had increased hepatic TG accumulation, but displayed repressed CREBH processing and reduced apoA-IV gene expression compared to controls. When deficient VLDL assembly in liver-specific MTP knockout mice was reconstituted by adenoviral infection with a human MTP transgene, steatosis-induced CREBH processing and apoA-IV expression were restored. In a mouse model of enhanced VLDL assembly (transgenic overexpression of human MTP), apoA-IV gene expression correlated with bulk hepatic TG accumulation, but not with VLDL secretion rate, indicating that other steatosis-related factors participate in apoA-IV gene regulation. Conclusions: Taken together, these data provide compelling evidence that VLDL assembly and secretion is required for hepatic CREBH processing and enhanced apoA-IV gene expression in the setting of acute steatosis. These data further suggest that CREBH and apoA-IV play central roles in VLDL-mediated hepatic lipid efflux.

This work was supported by the Foundation of the National Natural Science Foundation of China (grant numbers 20971054 and 90922034) and the Key Project of the Chinese Ministry of Education. The RU and UTD teams would like to acknowledge support from DOE (grant number DE-FG02-08ER46491). We thank Prof. Xianhe Bu and Dr. Ze Chang (Nankai University, China) and Dr. Ruiping Chen (Fujian Institute of Research on the Structure of Matter, Chinese Academy of Sciences) for part of the gas adsorption measurements.

Dysregulation of iron metabolism in cancer is well documented and it has been suggested that there is interdependence between excess iron and increased cancer incidence and progression. In an effort to better understand the linkages between iron metabolism and breast cancer, a predictive mathematical model of an expanded iron homeostasis pathway was constructed that includes species involved in iron utilization, oxidative stress response and oncogenic pathways. The model leads to three predictions. The first is that overexpression of iron regulatory protein 2 (IRP2) recapitulates many aspects of the alterations in free iron and iron-related proteins in cancer cells without affecting the oxidative stress response or the oncogenic pathways included in the model. This prediction was validated by experimentation. The second prediction is that iron-related proteins are dramatically affected by mitochondrial ferritin overexpression. This prediction was validated by results in the pertinent literature not used for model construction. The third prediction is that oncogenic Ras pathways contribute to altered iron homeostasis in cancer cells. This prediction was validated by a combination of simulation experiments of Ras overexpression and catalase knockout in conjunction with the literature. The model successfully captures key aspects of iron metabolism in breast cancer cells and provides a framework upon which more detailed models can be built., Author Summary Iron is required for cellular metabolism and growth, but can be toxic due to its ability to cause high oxidative stress and consequently DNA damage. To prevent damage, all organisms that require iron have developed mechanisms to tightly control iron levels. Dysregulation of iron metabolism is detrimental and can contribute to a wide range of diseases, including cancer. This paper presents a predictive mathematical model of iron regulation linked to iron utilization, oxidative stress, and the oncogenic response specific to normal breast epithelial cells. The model uses a discrete modeling framework to generate novel biological hypotheses for an investigation of how normal breast cells become malignant cells, capturing a breast cancer phenotype of iron homeostasis through overexpression and knockout simulations. The new biology discovered is (1) IRP2 overexpression alters the iron homeostasis pathway in breast cells, without affecting the oxidative stress response or oncogenic pathways, (2) an activated oncogenic pathway disrupts iron regulation in breast cancer cells.

From June to Oct. 1996, cage and field experiments with Fipronil, a new insecticide from the phenyl pyrazole family, were carried out in Hanzhong basin, Shaanxi Prov. The aim was to evaluate the action mode, persistence and control value of Fipronil in rice grasshoppers management. The main results were as follows: 1 at low doses of 4 g a. i. /ha and 8 g a. i. /ha, Fipronil was found to be an effective contact and stomach pesticide against Oxya spp. The knocking effect of contact was quicker than that of stomach; 2 the residual effect of Fipronil on Oxya spp. was over 3 weeks, significantly longer than that of conventional insecticides; 3 the difference between effects of 4 g a. i. /ha and 8 g a. i. /ha was mainly shown in terms of survival time of the grasshoppers after treatment, and there was almost no difference as to control results; 4 one month after the treatment, the density of Oxya in quadrats treated by Fipronil was significantly lower than that in quadrats treated with Fenpropathoursin, and the application of Fipronil retrieved 12. 6% of rice production loss when compared with the output in control field.

Iron is a metal essential for cellular metabolism. However, excess iron available for reactions contributes to the formation of dangerous reactive oxygen species, such as the hydroxyl radical, via the Fenton reaction. Therefore, intracellular iron levels are tightly constrained by a control system of proteins. This paper contains a mathematical model, in the form of a system of five ordinary differential equations, of the core of this control system, including the labile iron pool as well as proteins that regulate uptake, storage, and export and are connected through negative feedback loops. The model is validated using data from an overexpression experiment with cultured human breast epithelial cells. The parameters in the mathematical model are not known for this particular cell culture system, so the analysis of the model was done for a generic choice of parameters. Through a mixture of analytical arguments and extensive simulations it is shown that for any choice of parameters the model reaches a unique stable steady state, thereby ruling out oscillatory behavior. It is shown furthermore that the model parameters are identifiable through suitable experiments.

In this study, Al-MFI and B-MFI (Si/B = 100 and Si/B = 50) hollow fibres with nanocomposite architecture have been prepared on α-alumina by pore-plugging hydrothermal synthesis at 443 K for 89 h using a precursor clear solution with molar composition 1 SiO2: 0.45 TPAOH: 27.8 H2O: xH3BO3 (x = 0–0.02). The synthesized materials were characterized by XRD, SEM, ICP-AES and 29Si, 27Al- and 11B-MAS-NMR, revealing the genesis of well-intergrown materials with isomorphously substituted boron in the MFI unit cell. The pure ethylbenzene permeance within these membranes decreased in the order Al-MFI > B-MFI (Si/B = 50) > B-MFI (Si/B = 100). All the MFI materials were selective to p-xylene in the vapour permeation of ternary p-/m-/o-xylene mixtures and quaternary p-/m-/o-xylene/ethylbenzene model mixtures in the temperature range 400–650 K and for total feed vapour pressures lower than 4.5 kPa. The p-/m-xylene separation factor increased in the sense Al-MFI

Daramola, M. O. Deng, Z. Pera-Titus, M. Giroir-Fendler, A. Miachon, S. Burger, A. J. Lorenzen, L. Guo, Y.; International audience; In this paper, we present m-xylene isomerization in an extractor-type catalytic membrane reactor using nanocomposite MFI-alumina membrane tubes packed with a Pt-HZSM-5 catalyst. The catalytic performance of the membrane reactor was compared with that of a conventional fixed-bed reactor with similar dimensions and at comparable operation conditions. The influence of the reaction temperature, gas hourly space velocity, reaction time and reactor configuration on the performance of membrane reactor was explored. The membrane reactor displayed a maximum p-xylene yield of 5.1% at 523 K when computed at permeate-only mode, decreasing with temperature. At combined mode, the p-xylene yield was ca. 28%, showing an increase of about 18% compared to an equivalent fixed-bed reactor. The catalytic membrane reactor showed 100% selectivity towards p-xylene at permeate-only mode, displaying a maximum value of ca. 42% at 523 K at combined mode. Higher performance was obtained when the catalyst packing was close to the inner top layer of the membrane support. In this configuration, xylene permeate compositions higher than 95% could be achieved on the basis of the high p/o and p/m-xylene separation factors offered by the membrane. (C) 2010 Elsevier B.V. All rights reserved.

Deng, Z. Nicolas, C. -H. Daramola, M. O. Sublet, J. Schiestel, Th. Burger, A. J. Guo, Y. Giroir-Fendler, A. Pera-Titus, M.; International audience; One major drawback in the synthesis of zeolite membranes is the lack of reproducibility ascribed to the support quality. In this paper, a gas-liquid displacement technique was used prior to pore-plugging hydrothermal synthesis to evaluate the quality of hollow fibre supports in terms of pore size distribution of surface pores. Using these supports, four nanocomposite MFI-hollow fibre membrane families were identified, showing different gas/vapour separation performance. The effective MFI thickness of these membranes (0.6-1.2 mu m) was computed from pure N-2 and CO2 permeance using Maxwell-Stefan modelling, while their separation performance was evaluated in the separation of n-butane/H-2. CO2/N-2 and ternary xylene isomer mixtures. The MFI-alumina hollow fibres displaying the best quality corresponded to those synthesized using hollow fibres with surface pore size distributions centred at 0.2 mu m, suggesting more efficient pore plugging. Grain boundaries between nearby zeolite crystals only appear to play a role in the case of xylene isomer separation. (C) 2010 Elsevier B.V. All rights reserved.