The modification of surface basicity and its role in naphthalene oxidation: The effect of the basic sites introduced by Ce.

A series of V-xCe/Ti catalysts was prepared by a step impregnation method with gradual increased Ce amount. Compared to the commercial V-W/Ti catalysts, the V-xCe/Ti catalysts exhibited considerably higher COx selectivity during the oxidation of naphthalene (Nap), and less intermediates or by-products were detected both in gas phase and on the surface of the catalysts. Through a series of characterizations, it was found that abundance of weak basic sites in the form of OH was introduced by Ce, as well as the oxygen vacancies caused by the redox cycle of V4++Ce4+↔V5++Ce3+. The weak basic sites introduced by Ce could greatly enhance the Nap adsorption, and the Nap adsorbed was quickly converted to naphthol on Ce-OH. Furthermore, V existed at a high valence with the interaction of V and Ce, and the oxygen vacancies also increased the Oads and OOH. It improved the redox ability and the regeneration of Ce-OH on V-xCe/Ti catalysts. The intermediates could be further oxidized, and the Ce-OH consumed in the reaction could recover quickly. Therefore, almost 100% Nap conversion and a high COx selectivity was observed in the V-xCe/Ti catalysts system.

Simultaneous removal of naphthalene and NOx over V-Ce/Ti catalyst: Design of separated active sites for naphthalene degradation and SCR reaction.

V-Ce/Ti catalysts were prepared for the removal of naphthalene and NOx in the flue gas. The adverse effects of NH3 and NO on the naphthalene degradation were weakened on V-Ce/Ti, resulting in a decrease of only 2.5 % in COx selectivity. The formation of high molecular weight byproducts was also reduced. Besides the acid sites on the catalysts, Ce introduced new Brønsted basic sites, which could also adsorb and degrade naphthalene into naphthol effectively. With the separated active sites for naphthalene degradation and NO removal, the reaction between NH3 and the intermediates during the naphthalene degradation was also inhibited, decreasing the formation and accumulation of phthalimide. The oxidation of the intermediates was promoted by active V5+ introduced by Ce, inhibiting the transformation of the intermediates to higher molecular weight byproducts. Nearly 100 % conversion of naphthalene and NO, as well as 40.1 % of the COx selectivity were obtained on V-Ce/Ti.

Insights into the Efficient Release of the Polyacrylamide Drag Reducer via a pH-Responsive Inverse Polymer Emulsion.

The enormous demand for petroleum consumption has resulted in the shortage of fossil resources, prompting the need to explore unconventional reservoirs. Polyacrylamide emulsion drag reducers are capable of inhibiting the turbulence of fracturing fluids for enhancing the reservoir stimulation results, but the poor dissolution efficiency of polyacrylamide emulsion drag reducers is the primary limitation to their large-scale application. Here, a pH-responsive ionic liquid surfactant, oleic acid/cyclohexanediamine (HOA/HMDA), is synthesized by using oleic acid (HOA) and cyclohexanediamine (HMDA). HOA/HMDA shows a remarkable pH-responsive behavior due to the pH-induced deconstruction of the HOA/HMDA structure. Interestingly, the HOA/HMDA-stabilized monomer emulsion exhibits an obvious pH-induced emulsion structure transformation behavior. In addition, the HOA/HMDA-stabilized monomer emulsion possesses excellent dynamic and storage stability, supporting the inverse emulsion polymerization of the polymer P(AM/AMPS/AA). The obtained P(AM/AMPS/AA) polymer inverse emulsions maintained stability for 30 days. Our finding proposes that the structure of the P(AM/AMPS/AA) polymer inverse emulsions changes with pH stimulation, which is capable of facilitating the release of polymers. P(AM/AMPS/AA) is released from the P(AM/AMPS/AA) polymer inverse emulsions within 30 s at a pH value of 12.06, along with a drag reduction rate of 62.54%. Obviously, the HOA/HMDA-stabilized P(AM/AMPS/AA) polymer inverse emulsions eliminate the contradiction between the stability and release of polyacrylamide emulsion drag reducers, which is promising for meeting the demands of reservoir stimulation.

A method for evaluating the safety of freeway tunnel sections based on driving comfort - a naturalistic driving study.

OBJECTIVE: Driving comfort is crucial for tunnel safety because tunnel sections on freeways often introduce significant environmental changes that can compromise comfort and increase the risk of traffic accidents. This study aimed to quantitatively evaluate the driving comfort in tunnel sections and its implications for safety management. METHODS: Four indicators were used to assess the driving comfort: heart rate growth rate (Hrgr), skin conductance response (SCR), speed, and acceleration. The CRITIC weighting method was employed to calculate a quantitative driving comfort score, and the presence and severity of discomfort were used to evaluate the safety of each tunnel area. In addition, the evaluation was based on a naturalistic test consisting of Hrgr, SCR, speed, and acceleration data. A total of 32 participants were recruited based on a web-based questionnaire screening process, after which they were tested while driving through 30 tunnel sections on the roadway. These 30 tunnels included 14 short (< 500 m), 12 medium (500-1,000 m), and 4 long (1,000-3,000 m) tunnels. RESULTS: The results revealed that the four selected indicators exhibited minimal multicollinearity and effectively captured the driving comfort. Among the indicators, SCR had the most significant contribution to the driving comfort score. Most drivers did not experience substantial discomfort while driving through tunnels. The area where drivers were most susceptible to discomfort was the middle zones of tunnels. However, drivers were more likely to experience strong discomfort in the outside exit, entrance, and middle zones of short, medium, and long tunnels, respectively. CONCLUSIONS: This study provides a comprehensive set of safety evaluation methods for tunnel sections on freeways, with a focus on quantifying the driving comfort. The findings provide theoretical support for freeway management personnel in implementing personalized controls in different tunnel areas with the aim of enhancing tunnel safety and mitigating the occurrence of traffic accidents.

Plasma-Catalytic CO2 Hydrogenation over a Pd/ZnO Catalyst: In Situ Probing of Gas-Phase and Surface Reactions.

Plasma-catalytic CO2 hydrogenation is a complex chemical process combining plasma-assisted gas-phase and surface reactions. Herein, we investigated CO2 hydrogenation over Pd/ZnO and ZnO in a tubular dielectric barrier discharge (DBD) reactor at ambient pressure. Compared to the CO2 hydrogenation using Plasma Only or Plasma + ZnO, placing Pd/ZnO in the DBD almost doubled the conversion of CO2 (36.7%) and CO yield (35.5%). The reaction pathways in the plasma-enhanced catalytic hydrogenation of CO2 were investigated by in situ Fourier transform infrared (FTIR) spectroscopy using a novel integrated in situ DBD/FTIR gas cell reactor, combined with online mass spectrometry (MS) analysis, kinetic analysis, and emission spectroscopic measurements. In plasma CO2 hydrogenation over Pd/ZnO, the hydrogenation of adsorbed surface CO2 on Pd/ZnO is the dominant reaction route for the enhanced CO2 conversion, which can be ascribed to the generation of a ZnO x overlay as a result of the strong metal-support interactions (SMSI) at the Pd-ZnO interface and the presence of abundant H species at the surface of Pd/ZnO; however, this important surface reaction can be limited in the Plasma + ZnO system due to a lack of active H species present on the ZnO surface and the absence of the SMSI. Instead, CO2 splitting to CO, both in the plasma gas phase and on the surface of ZnO, is believed to make an important contribution to the conversion of CO2 in the Plasma + ZnO system.

High-fat diet-induced hyperinsulinemia promotes the development of prostate adenocarcinoma in prostate-specific Pten-/- mice.

Metabolic syndrome (MetS) and its four clinical entities, central obesity, insulin resistance, hypertension and dyslipidemia, are implicated in increasing the risk and mortality of cancer in several organs. However, it is unclear how they are associated with increased risk of prostate cancer. To elucidate the mechanistic link between MetS and prostate carcinogenesis, we characterized the development of MetS and prostate adenocarcinoma in prostate-specific Pten-/- (Ptenp-/-) mice fed a high-fat (HF) diet. We found that male Ptenp-/- mice on an HF diet gained excess body weight and elevated blood glucose, insulin and insulin-like growth factor 1 (IGF1) levels at 20 weeks of age and were obese at 40 weeks. Prostate adenocarcinoma multiplicity at 40 weeks was significantly higher in the mice on an HF diet, suggesting that the HF diet promotes the development of prostate adenocarcinoma. Increased cell proliferation and enhanced AKT activation were found in the prostates of mice on an HF diet. Further transcriptome study revealed that receptor tyrosine kinase regulation, which mediates insulin/IGF1 signaling, was one of the top enriched pathways by HF diet-induced transcriptome changes. Together, our results suggest that HF diet-induced hyperinsulinemia leads to increased activation of insulin/IGF1/AKT signaling in lesioned prostates, promoting the development of adenocarcinoma.

δ-Tocotrienol is the Most Potent Vitamin E Form in Inhibiting Prostate Cancer Cell Growth and Inhibits Prostate Carcinogenesis in Ptenp-/- Mice.

Vitamin E compounds, consisting of α, ß, γ, and δ forms of tocopherols and tocotrienols, display different cancer preventive activities in experimental models. Tocotrienols may have higher potential for clinical use due to their lower effective doses in laboratory studies. However, most studies on tocotrienols have been carried out using cancer cell lines. Strong data from animal studies may encourage the use of tocotrienols for human cancer prevention research. To examine the cancer inhibitory activity of different vitamin E forms, we first investigated their inhibitory activities of different vitamin E forms in prostate cancer cell lines. We found that δ-tocotrienol (δT3) was the most effective form in inhibiting cell growth at equivalent doses. Because of this in vitro potency, δT3 was further studied using prostate-specific Pten-/- (Ptenp-/-) mice. We found that 0.05% δT3 in diet reduced prostate adenocarcinoma multiplicity by 32.7%, featuring increased apoptosis and reduced cell proliferation. The inhibitory effect of 0.05% δT3 in diet was similar to that of 0.2% δ-tocopherol (δT) in diet reported previously. Our further study on the δT3-induced transcriptome changes indicated that δT3 inhibited genes in blood vessel development in the prostate of Ptenp-/- mice, which was confirmed by IHC. Together, our results demonstrate that δT3 effectively inhibits the development of prostate adenocarcinoma in Ptenp-/- mice, which involves inhibition of proliferation and angiogenesis and promotion of apoptosis. PREVENTION RELEVANCE: We demonstrated that δ-tocotrienol is the most active vitamin E form in inhibiting the growth of several prostate cancer cell lines. In transgenic Ptenp-/- mice, δ-tocotrienol inhibited the formation of prostate cancer. This result would encourage and help design clinical studies for the application of δ-tocotrienol for prostate cancer prevention.

Tuning the local electronic structure of SrTiO3 catalysts to boost plasma-catalytic interfacial synergy.

Boosting plasma-catalyst synergy to enhance volatile organic compounds (VOCs) decomposition remains a challenge. Herein, rich oxygen vacancies (VO) were engineered into the SrTiO3 catalysts through a facile nitrogen incorporation strategy for the plasma-catalytic decomposition of toluene and ethyl acetate. 100% toluene conversion with 81% CO2 selectivity at a competitive energy efficiency was achieved under ambient conditions. The characterization results and theoretical calculations evidenced that the partial substitution of oxygen by nitrogen triggered the electronic reconstruction and local disorder, thus modulating the electronic properties and coordination structures contributed to the formation of VO-Ti3+ pairs. Quasi in-situ EPR, operando OES, and operando DRIFTS originally demonstrated that the VO-Ti3+ pairs as active sites promoted the plasma-catalytic synergy instead of isolated VO. Importantly, the VO-Ti3+ pairs with favorable electron transfer characteristics energetically preferred to capture and utilize vibrationally excited oxygen species. And the lattice oxygen supplied by the VO-Ti3+ pairs were more vigorously activated by the plasma to participate in the surface/interface reaction. This work advances our understanding of the real active sites in plasma-catalytic interfacial synergy and thus paving the way for the rational design of efficiently heterogeneous catalysts.

In-situ atmosphere thermal pyrolysis of spindle-like Ce(OH)CO3 to fabricate Pt/CeO2 catalysts: Enhancing Pt-O-Ce bond intensity and boosting toluene degradation.

In this work, a series of spindle-like CeO2 supports with different contents of surface oxygen vacancies were fabricated by an in-situ atmosphere thermal pyrolysis method. Due to the unique surface physicochemical properties of the modified CeO2 supports, the interaction between Pt and CeO2 can be regulated during the synthesis of the Pt/CeO2 catalyst. The abundant oxygen vacancies on the CeO2 support could preferentially trap Pt2+ ions in solution during the Pt impregnation process and enhance the Pt-CeO2 interaction in the subsequent reduction process, which results in the strongest Pt-O-Ce bonds formed on the PCH catalysts successfully (0.6% Pt loading on the CH support, which generated by thermal pyrolysis of Ce(OH)CO3 under H2 atmosphere). The strong Pt-O-Ce bond would trigger abundant surface oxygen species generated and enhanced the lattice oxygen species transfer from CeO2 supports to Pt nanoparticles. It was crucial to boosting the toluene catalytic activity. Therefore, the PCH catalyst exhibits the highest activity for toluene oxidation (T10 = 120 °C, T50 = 138 °C, and T90 = 150 °C with WHSV = 60,000 mL g-1 h-1) and remarkable durability and water resistance among all catalysts. We also conclude that the Pt-O-Ce bond may be the active site for toluene oxidation by calculating the turnover frequencies (TOFPt-O-Ce) value for all Pt/CeO2 catalysts. Moreover, the DFT calculation indicates that the Pt/CeO2 catalyst with a strong Pt-O-Ce bond possesses the lowest oxygen absorption energy and higher CO tolerance ability, which leads to excellent catalytic performance for toluene and CO catalytic oxidation.

Colitis-induced IL11 promotes colon carcinogenesis.

Colitis increases the risk of colorectal cancer; however, the mechanism of the association between colitis and cancer remains largely unknown. To identify colitis-associated cancer promoting factors, we investigated gene expression changes caused by dextran sulfate sodium (DSS)-induced colitis in mice. By analyzing gene expression profiles, we found that IL11 was upregulated in DSS-induced colitis tissue and 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP)/DSS-induced colon tumours in mice as well as in human colorectal cancer. By characterizing the activation/phosphorylation of STAT3 (pSTAT3), we found that pSTAT3 was induced transiently in colitis, but maintained at higher levels from hyper-proliferative dysplastic lesions to tumours. Using the IL11 receptor (IL11Rα1) knockout mice, we found that pSTAT3 in the newly regenerated crypt epithelial cells in colitis is abolished in IL11Rα1+/- and -/- mice, suggesting that colitis-induced IL11 activates STAT3 in colon crypt epithelial cells. Moreover, colitis-promoted colon carcinogenesis was significantly reduced in IL11Rα1+/- and -/- mice. To determine the roles of the IL11 in colitis, we found that the inhibition of IL11 signalling by recombinant IL11 antagonist mutein during colitis was sufficient to attenuate colitis-promoted carcinogenesis. Together, our results demonstrated that colitis-induced IL11 plays critical roles in creating cancer promoting microenvironment to facilitate the development of colon cancer from dormant premalignant cells.

Nonthermal plasma catalysis for toluene decomposition over BaTiO3-based catalysts by Ce doping at A-sites: The role of surface-reactive oxygen species.

The insights on the primary surface-reactive oxygen species and their relation with lattice defects is essential for designing catalysts for plasma-catalytic reactions. Herein, a series of Ba1-xCexTiO3 perovskite catalysts with high specific surface areas (68.6-85.6 m2 g-1) were prepared by a facile in-situ Ce-doping strategy and investigated to catalytically decompose toluene. Combining the catalysts with a nonthermal plasma produced a significant synergy effect. The highest decomposition efficiency (100%), COx selectivity (98.1%), CO2 selectivity (63.9%), and the lowest O3 production (0 ppm) were obtained when BC4T (Ce/Ti molar ratio = 4:100) was packed in a coaxial dielectric barrier discharge reactor at a specific input energy of 508.8 J L-1. The H2-TPR, temperature-programmed Raman spectra, EPR and OSC results suggested that superoxides (•O2-) were the primary reactive oxygen species and were reversibly generated on the perovskite surface. Molecular O2 was adsorbed and activated at the active sites (Ti3+-VO) via an electron transfer process to form •O2-. Surface-adsorbed •O2- had a greater effect on the heterogeneous surface plasma reactions than the dielectric constant, and enhanced the toluene decomposition and intermediate oxidation. A possible reaction path of toluene decomposition was also proposed.

Morphology-activity correlation of electrospun CeO2 for toluene catalytic combustion.

Herein, CeO2 catalysts with nanotube, nanobelt, and wire-in-nanotube morphologies were successfully fabricated by a facile single spinneret electrospinning technique. And catalytic activity of these electrospun CeO2 nanomaterials were evaluated by toluene catalytic combustion reaction. Among the three morphologies of CeO2 catalysts, CeO2 nanobelt (CeO2-NB) presented the best toluene catalytic combustion performance (T90% = 230 °C) at WHSV = 60,000 mL g-1 h-1, also exhibited the lowest activation energy (Ea = 80.2 kJ/mol). Based on the characterization by TEM, XRD, BET, SEM, XPS, Raman spectroscopy, H2-TPR, and O2-TPD results, the high catalytic activity of CeO2-NB catalyst was attributed to its porous nanobelt morphology with larger specific surface area and the abundance of surface oxygen vacancies. Furthermore, the CeO2-NB catalysts presented an excellent durability by longtime on-stream test (as well as presence of 5% vol. water vapor), suggesting its great potential for practical air pollution control application.

Vertically-aligned Co3O4 arrays on Ni foam as monolithic structured catalysts for CO oxidation: effects of morphological transformation.

A generic hydrothermal synthesis route has been successfully designed and utilized to in situ grow highly ordered Co3O4 nanoarray (NA) precursors on Ni substrates, forming a series of Co3O4 nanoarray-based monolithic catalysts with subsequent calcination. The morphology evolution of Co3O4 nanostructures which depends upon the reaction time, with and without CTAB or NH4F is investigated in detail, which is used to further demonstrate the growth mechanism of Co3O4 nanoarrays with different morphologies. CO is chosen as a probe molecule to evaluate the catalytic performance over the synthesized Co-based oxide catalysts, and the effect of morphological transformation on the catalytic activity is further confirmed via using TEM, H2-TPR, XPS, Raman spectroscopy and in situ Raman spectroscopy. As a proof of concept application, core-shell Co3O4 NAs-8 presenting hierarchical nanosheets@nanoneedle arrays with a low density of nanoneedles exhibits the highest catalytic activity and long-term stability due to its low-temperature reducibility, the lattice distortion of the spinel structure and the abundance of surface-adsorbed oxygen (Oads). It is confirmed that CO oxidation on the surface of Co3O4 can proceed through the Langmuir-Hinshelwood mechanism via using in situ Raman spectroscopy. It is expected that the in situ synthesis of well-defined Co3O4 monolithic catalysts can be extended to the development of environmentally-friendly and highly active integral materials for practical industrial catalysis.

Formation of persistent hyperplastic primary vitreous in ephrin-A5-/- mice.

PURPOSE: Primary vitreous regression is a critical event in mammalian eye development required for proper ocular maturity and unhindered vision. Failure of this event results in the eye disease persistent hyperplastic primary vitreous (PHPV), also identified as persistent fetal vasculature (PFV), a condition characterized by the presence of a fibrovascular mass adjacent to the lens and retina, and associated with visual disability and blindness. Here, we identify ephrin-A5 to be a critical regulator for primary vitreous regression. METHODS: Wild-type and ephrin-A5(-/-) eyes were examined at various developmental stages to determine the progression of PHPV. Eye tissue was sectioned and examined by H&E staining. Protein expression and localization was determined through immunohistochemistry. Relative levels of Eph receptors were determined by RT-PCR. RESULTS: Ephrin-A5(-/-) animals develop ocular phenotypes representative of PHPV, most notably the presence of a large hyperplastic mass posterior to the lens that remains throughout the lifetime of the animal. The aberrant tissue in these mutant mice consists of residual hyaloid vessels surrounded by pigmented cells of neural crest origin. Labeling with bromodeoxyuridine (BrdU) and detection of proliferating cell nuclear antigen (PCNA) expression shows that the mass in ephrin-A5(-/-) animals is mitotically active in embryonic and postnatal stages. CONCLUSIONS: Ephrin-A5 is a critical factor that regulates primary vitreous regression.

Further analysis of the lens of ephrin-A5-/- mice: development of postnatal defects.

PURPOSE: The cells of the mammalian lens must be carefully organized and regulated to maintain clarity. Recent studies have identified the Eph receptor ligand ephrin-A5 as a major contributor to lens development, as mice lacking ephrin-A5 develop abnormal lenses, resulting in cataracts. As a follow-up to our previous study on the cataracts observed in ephrin-A5(-/-) animals, we have further examined the morphological and molecular changes in the ephrin-A5(-/-) lens. METHODS: Wild-type and ephrin-A5(-/-) eyes at various ages were fixed, sectioned, and examined using histological techniques. Protein expression and localization were determined using immunohistochemistry and western blot analysis. RESULTS: Lens abnormalities in the ephrin-A5(-/-) animals are observed at postnatal stages, with lens opacity occurring by postnatal day 21. Structural defects in the lens are first observed in the outer lens fiber cell region where cells in the ephrin-A5(-/-) lens are severely disorganized. Ephrin-A5 and the Eph receptor EphA2 are expressed during early ocular development and continue to be expressed into postnatal stages. The cataracts in the ephrin-A5(-/-) mutants occur regardless of the presence of the CP49 mutation. CONCLUSIONS: In this follow-up study, we have uncovered additional details explicating the mechanisms underlying ephrin-A5 function in the lens. Furthermore, elucidation of the expression of ephrin-A5 and the Eph receptor EphA2 in the lens supports a fundamental role for this receptor-ligand complex in lens development. These observations, in concert with our previous study, strongly suggest that ephrin-A5 has a critical role in postnatal lens fiber organization to maintain lens transparency.

Deleterious effects of high concentrations of (-)-epigallocatechin-3-gallate and atorvastatin in mice with colon inflammation.

Epigallocatechin-3-gallate (EGCG), atorvastatin (ATST), and their combination have been previously shown to inhibit colon carcinogenesis in animal models. We further investigated their inhibitory activities in azoxymethane (AOM) and dextran sulfate sodium (DSS)-treated Balb/cJ mice and CD-1 mice in 2 slightly different models. The mice were maintained on the AIN93M diet, or a similar diet containing 0.03%, 0.1%, or 0.3% EGCG; 60-ppm ATST; or a combination of 0.1% EGCG and 60-ppm ATST. Unexpectedly, no significant inhibitory activity was observed, and some of the treatment groups resulted in higher tumor multiplicity. To study the effects of EGCG on colon inflammation, CD-1 or C57BL/6 mice were treated with 1.5% DSS for 7 days and sacrificed 3 days later. DSS induced rectal bleeding and colon shortening; treatment with 0.5% EGCG exacerbated the bleeding and decreased mouse body weight. Dietary 0.5% EGCG also increased serum levels of leukotriene B4 and prostaglandin E2. These results suggest that, in mice bearing colon inflammation, high concentrations of EGCG and ATST enhance colon bleeding and may promote colon carcinogenesis.

Loss of ephrin-A5 function disrupts lens fiber cell packing and leads to cataract.

Cell-cell interactions organize lens fiber cells into highly ordered structures to maintain transparency. However, signals regulating such interactions have not been well characterized. We report here that ephrin-A5, a ligand of the Eph receptor tyrosine kinases, plays a key role in lens fiber cell shape and cell-cell interactions. Lens fiber cells in mice lacking ephrin-A5 function appear rounded and irregular in cross-section, in contrast to their normal hexagonal appearance in WT lenses. Cataracts eventually develop in 87% of ephrin-A5 KO mice. We further demonstrate that ephrin-A5 interacts with the EphA2 receptor to regulate the adherens junction complex by enhancing recruitment of beta-catenin to N-cadherin. These results indicate that the Eph receptors and their ligands are critical regulators of lens development and maintenance.

Inhibition of intestinal tumorigenesis in Apc(min/+) mice by green tea polyphenols (polyphenon E) and individual catechins.

In this work, we compared the cancer preventive activities of Polyphenon E (PPE), a standardized green tea polyphenol preparation given in diet versus drinking fluid as well as the activities of PPE versus individual catechins. We treated Apc(Min/+) mice for 9 wk with 0.08% (-)-epigallocatechin-3-gallate (EGCG), 0.08% (-)-epicatechin-3-gallate, or 0.12% PPE in drinking fluid or diet. Only 0.12% dietary PPE and 0.08% EGCG in drinking fluid significantly decreased tumor multiplicity (70% and 51%, respectively). Compared to PPE in drinking fluid, dietary PPE delivered twofold more EGCG to the small intestine. Immunohistochemistry showed that adenomas in groups treated with PPE and EGCG had decreased cell proliferation, Beta -catenin nuclear expression, and phospho-Akt levels; higher cleaved caspase-3 levels, and partially restored retinoid X receptor alpha expression. The results suggest that these molecular events contribute to the cancer prevention activity of EGCG and PPE. Furthermore, diet appears to be a better route of administration for PPE than drinking fluid.

Interaction between proteins and cationic gemini surfactant.

Surface tension, fluorescence, and circular dichroism (CD) methods have been used to investigate the interaction between cationic gemini surfactant 1,2-ethane bis(dimethyldodecylammonium bromide) (C12C2C12) and proteins including bovine serum albumin (BSA) and gelatin. Surface tension measurements show that the complexes of gelatin--C12C2C12 form more easily than that of BSA--C12C2C12. Addition of C12C2C12 has a different effect not only on the polarity of the microenvironment in BSA and gelatin systems but also on their fluorescence spectra. It can be seen from far-UV CD spectra that the alpha-helical network of BSA is disrupted and its content decreases from 41.7% to 27.6% while the random coil content of gelatin increases from 53.0% to 55.9% with increasing C12C2C12 concentration. The results from near-UV CD spectra show that the binding of C12C2C12 induces changes of the microenvironment around the aromatic amino acid residues and disulfide bonds of BSA at high C12C2C12 concentrations.

Inhibition of lung carcinogenesis and effects on angiogenesis and apoptosis in A/J mice by oral administration of green tea.

Oral administration of tea (Camellia sinensis) has been shown to inhibit the formation and growth of several tumor types in animal models. The present study investigated the effects of treatment with different concentrations of green tea on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in female A/J mice. Two days after a single dose of NNK (100 mg/kg body weight, i.p.), the mice were given 0.1, 0.2, 0.4, and 0.6% green tea solution (1, 2, 4, and 6 g of tea solids, respectively, dissolved in 1 l of water), 0.02% caffeine, or water as the sole source of drinking fluid until the termination of the experiment. Only the treatment with 0.6% tea preparation significantly reduced lung tumor multiplicity (mean +/- SE, 6.07 +/- 0.77 vs. 8.60 +/- 0.50 tumors per mouse, P = 0.018). Treatment with 0.6% tea also inhibited angiogenesis, as indicated by the lower microvessel density (number of blood vessels/mm2) based on immunostaining for the von Willebrand factor antigen (81.9 +/- 9.5 vs. 129.4 +/- 8.2, P = 0.0018) and anti-CD31 antibody staining (465.3 +/- 61.4 vs. 657.1 +/- 43.6, P = 0.0012). Significantly lower vascular endothelial growth factor immunostaining scores were also observed in the 0.6% tea-treated group (0.98 +/- 0.17 vs. 1.43 +/- 0.07, P = 0.006). The apoptosis index was significantly higher in lung adenomas from 0.6% tea-treated mice based on morphological analysis of cell apoptosis (2.51 +/- 0.18% vs. 1.57 +/- 0.11%, P = 0.00005), and the result was further confirmed using the TUNEL method. Inhibition of angiogenesis and the induction of apoptosis by green tea may be closely related to the inhibition of pulmonary carcinogenesis.