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New sol-gel precursors having the ability to protect iron against corrosion were synthesized and used to prepare organic-inorganic hybrid coatings based on epoxy. Bisphenol A epoxy was modified with 3-isocyanatopropyltriethoxysilane to improve the compatibility, and water and HCl were used as catalysts for sol-gel process. Various coating formulations were prepared depending on the type of sol-gel precursors and the amount of each ingredient, and cast on iron substrates by dip-coating and thermally cured. Corrosion protection properties of coated iron were studied by a salt spray test and electrochemical impedance spectroscopy under 0.1 M NaCl electrolyte. Hybrid coatings containing anticorrosive functional group exhibited excellent corrosion protection on iron, compared to that of typical hybrid coatings. From electrochemical impedance spectroscopy, the hybrid coatings containing anticorrosive functional group could maintaine the initial impedance after 500 h, while the impedance of hybrid coatings without them started to decrease after 24 h.

We report the effect of the amount of the mesoporous material, SBA-15, on the basic traits of fully aliphatic polyimides (API). For this purpose, water soluble, fully aliphatic poly(amic acid) triethyl amine salts (PAA(s)) were prepared and mixed with various amounts of SBA-15. Fully aliphatic polyimide hybrid composites containing the SBA 15-type mesoporous silica were synthesized successfully from bicyclo [2.2.2] oct-7-ene-2,3,5,6-tetracarboxylic dianhydride and alicyclic diamine, 4,4′-methylene bis(2-methylcyclohexylamine). The structure of the hybrid composites was confirmed by IR spectroscopic analysis. Scanning electron microscopy revealed the morphology of the compounds. The hybrid composites exhibited good thermal stability, reasonable transparency, and a low dielectric constant.

Polyimide (PI) multilayer thin films were prepared by spin-coating from a poly(amic acid) (PAA) and poly(amic acid) ammonium salt (PAAS). PI was prepared from pyromellitic dianhydride (PMDA) and 4,4′-oxydianiline (ODA) PAA. Different compositions of PAAS were prepared by incorporating triethylamine (TEA) into PMDA-ODA PAA in dimethylacetamide. PI multilayer thin films were spin-coated from PMDA-ODA PAA and PAAS. The PAAS comprising cationic and anionic moieties were spherical with a particle size of 20≈40 nm. Some particles showed layers with ammonium salts, despite poor ordering. Too much salt obstructed the interaction between the polymer chains and caused phase separation. A small amount of salt did not affect the interactions of the interlayer structure but did interrupt the stacking between chains. Thermogravimetric analysis (TGA) showed that the average decomposition temperature of the thin films was 611 °C. All the films showed almost single-step, thermal decomposition behavior. The nanostructure of the multilayer thin films was confirmed by X-ray reflectivity (XRR). The LF 43 film, which was prepared with a 4:3 molar ratio of PMDA and ODA, was comprised of uniformly spherical PAAS particles that influenced the nanostructure of the interlayer by increasing the interaction forces. This result was supported by the atomic force microscopy (AFM) data. It was concluded that the relationship between the uniformity of the PAAS particle shapes and the interaction between the layers affected the optical and thermal properties of PI layered films.

In the past few decades, the use of natural compounds, such as flavonoids, as anti-inflammatory agents has gained much attention. Our current study focuses on the preventive effects of quercetin, apigenin, and luteolin on cytokine-induced beta-cell damage.Pancreatic beta-cells or islets were treated with cytokine mixtures in the presence or absence of flavonoids and the inhibitory effect of flavonoids against cytokine toxicity was determined.Treatment of RINm5F (RIN) rat insulinoma cells with interleukin 1beta (IL-1beta) and interferon gamma (IFN-gamma) induced cell damage. Quercetin, apigenin, and luteolin completely protected against IL-1beta- and IFN-gamma-mediated cytotoxicity in RIN cells. Incubation with quercetin, apigenin, and luteolin resulted in a significant reduction in IL-1beta- and IFN-gamma-induced nitric oxide production, a finding that correlated well with reduced levels of the inducible form of NO synthase messenger RNA and protein. The molecular mechanism by which quercetin, apigenin, and luteolin inhibited inducible NO synthase gene expression appeared to involve the inhibition of nuclear factor kappaB (NF-kappaB) activation. The IL-1beta- and IFN-gamma-stimulated RIN cells showed increases in NF-kappaB binding activity, p50 and p65 subunit levels in nucleus, and IkappaB alpha degradation in cytosol compared with unstimulated cells. Quercetin, apigenin, and luteolin also prevented IL-1beta- and IFN-gamma-mediated inhibition of insulin secretion.Quercetin, apigenin, and luteolin inhibited cytotoxicity in RIN cells and attenuated the decrease of glucose-stimulated insulin secretion in islets by IL-1beta and IFN-gamma.

We demonstrated previously that Coptidis rhizoma extract (CRE) prevented S-nitroso-N-acetylpenicillamine-induced apoptotic cell death via the inhibition of mitochondrial membrane potential disruption and cytochrome c release in RINm5F (RIN) rat insulinoma cells. In this study, the preventive effects of CRE against cytokine-induced beta-cell death was assessed. Cytokines generated by immune cells infiltrating pancreatic islets are crucial mediators of beta-cell destruction in insulin-dependent diabetes mellitus. The treatment of RIN cells with IL-1beta and IFN-gamma resulted in a reduction of cell viability. CRE completely protected IL-1beta and IFN-gamma-mediated cell death in a concentration-dependent manner. Incubation with CRE induced a significant suppression of IL-1beta and IFN-gamma-induced nitric oxide (NO) production, a finding which correlated well with reduced levels of the iNOS mRNA and protein. The molecular mechanism by which CRE inhibited iNOS gene expression appeared to involve the inhibition of NF-kappaB activation. The IL-1beta and IFN-gamma-stimulated RIN cells showed increases in NF-kappaB binding activity and p65 subunit levels in nucleus, and IkappaB alpha degradation in cytosol compared to unstimulated cells. Furthermore, the protective effects of CRE were verified via the observation of reduced NO generation and iNOS expression, and normal insulin-secretion responses to glucose in IL-1beta and IFN-gamma-treated islets.

The environmental-compatible epoxy resins/clay nanocomposites were prepared by using epoxidized castor oil (ECO) and two ion-exchanged clays. The glass transition temperature (Tg) and mechanical interfacial properties of ECO/clay nanocomposites were investigated. As a result, the nanocomposites showed higher Tg than that of neat ECO. The mechanical interfacial properties of both the nanocomposites were significantly increased on increasing the clay content.

A various organic modifiers depending on the substituents of ammonium ions were synthesized and used to prepare organically modified montmorillonite (OMMT). Nitrile-butadiene rubber (NBR)/OMMT nanocomposites could be obtained using melt-compounding followed by hot-press vulcanization. d-Spacings of OMMT were changed as the chemical structures of modifiers were varied. X-ray diffraction (XRD) and tensile measurements of NBR nanocomposites revealed that the structures of organic modifiers affect the properties of NBR nanocomposites after vulcanization. Long alkyl chain of OMMT induced higher interaction between NBR and OMMT, resulting in higher tensile strength, Young’s modulus, and hardness of NBR/OMMT nanocomposites.

Styrene-butadiene rubber (SBR) nanocomposites were prepared from organically modified montmorillonite (OMMT). To enhace the dispersion properties of OMMT in SBR matrix, polybutadiene was modified with tetramethyl siloxane substituted with benzylamine, and the master batches of those were prepared by a solution process using tetrahydrofuran. SBR/master batch nanocomposites could be obtained by melt-compounding followed by hot-press vulcanization. Xray diffraction (XRD) studies revealed that the interlayer distances of OMMT were increased and the nanocomposites had the intercalated and exfoliated structures of OMMT by the nanocomposition of SBR with the master batch. Mechanical and dispersion properties of the nanocomposites from the master batch are superior to those of nanocomposites without master batch.

Zirconium based thin film have been deposited by atomic layer deposition (ALD) process using Zr and Si containing Zr precursor with ozone as oxidant. We have pursued a means to control composition by varying Zr and Si containing precursor by cycle frequency. The molar ratio of Si to Zr in the Zr based films was 0.2, 0.25, 0.33, and 0.5. Addition of Si containing Zr precursor on Zirconium based thin films was effective for the decrease of the roughness, while an increase of density. XPS analysis indicated that the addition of Si containing Zr precursors in the Zr based film formed the silicate structure. The XRD analysis of the all ZrO2-SiO2 mixed films annealed at 600 degrees C for 5 min indicated the presence of amorphous. However, the ZrO2 film showed diffraction peaks at 2θ = 30.6 degrees due to the presence of the Tetragonal ZrO2. The incorporation of Si into ZrO2 films helps stabilize an amorphous structure during deposition and annealing. The Zr based thin film (Si/Zr = 0.25) exhibited that the leakage current density was 6.2 x 10(-7) A/cm2 at a bias of - 1.5 V.

Radix Paeoniae Alba has been used as a constituent of herbal medicine prescriptions for the treatment of inflammation, cancer, and other diseases. The aim of this study was to investigate the mechanism of Radix Paeoniae Alba extract (RPAE)-induced apoptosis in HL-60 leukemic cells. We observed that RPAE induced apoptotic changes in a dose-dependent manner, which was confirmed by DNA fragmentation and poly-(ADP-ribose) polymerase (PARP) cleavage. We also found release of cytochrome c from mitochondria to the cytosol in RPAE-treated HL-60 cells. The caspases, caspase-9 and -3, but not caspase-8, were found to be activated in response to RPAE treatment, and the caspase-3 inhibitor, Ac-DEVD-CHO, and the caspase-9 inhibitor, z-LEHD-FMK, but not the caspase-8 inhibitor, z-IETD-FMK, attenuated RPAE-induced DNA fragmentation and PARP cleavage. These results suggest that RPAE-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and via a caspase-3 dependent mechanism.

A bismaleimide (BMI) resin was added to an epoxy system composed of N,N′-tetraglycidyldiaminodiphenyl methane (TGDDM) and diaminodiphenyl methane (DDM). Cure behavior of the BMI modified epoxy resins was studied by a dynamic differential scanning calorimetry (DSC) method. Dynamic DSC thermograms of the BMI modified epoxy resins indicated unimodal reaction exothermic peaks. The overall heat of reaction per unit mass decreased with BMI composition. The residual heat of reactions of the epoxy blends cured at 180°C for 3 h increased with BMI composition. Thermal stability of the epoxy system improved by incorporating BMI resin. Flexural strength and modulus increased with BMI composition.

Scutellaria barbata has been used to treat cancer in Chinese medicine. The responsible anticancer mechanism, however, is not clear. Here we demonstrated an inhibitory mechanism due to a Scutellaria barbata extract (SBE) on a human promyelocytic leukemia cell line (HL-60) that has a mutation in the tumor suppressor gene p53. HL-60 cells were incubated with various concentrations of SBE. After a 24-h incubation, cytotoxicity and apoptosis were determined by MTT and DNA fragmentation assay, respectively. After treatment with SBE, cell cycle arrest was determined by measuring the cell number stained by 5'-bromo-2'-deoxyuridine (BrdU) and 7-amino-actinomycin D (7-AAD). Treatment of cells with SBE resulted in a concentration- and time-dependent inhibition of growth and a G 1 phase arrest of the cell cycle. This effect was associated with a marked decrease in the protein expression of cyclin A, D 1 , D2, D3, and E and their activating partners, cyclin-dependent kinases (CDK) 2, 4, and 6 with concomitant upregulation of p21, cyclin-dependent kinase inhibitor. Downstream of the CDK inhibitory protein-CDK/cyclin cascade, SBE decreased phosphorylation level of retinoblastoma protein. SBE treatment also resulted in apoptosis evidenced by an increase of sub-G 1 phase cells, DNA fragmentation and degradation of the inhibitory protein for the caspase-activated deoxyribonuclease. The molecular mechanism during SBE-mediated growth inhibition in HL-60 cells may be due to modulation of the cell-cycle machinery and the induction of apoptosis.

Cytokines produced by immune cells infiltrating pancreatic islets are important mediators of beta-cell destruction in insulin-dependent diabetes mellitus. Cytokines stimulate an inducible form of nitric oxide synthase (iNOS) expression and nitric oxide (NO) production, leading to insulin insufficiency. In the present study, the effects of Artemisia capillaris extract (ACE) on cytokine-induced beta-cell damage were examined. Treatment of RINm5F (RIN) rat insulinoma cells with interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma) induced cell damage. ACE completely protected IL-1beta and IFN-gamma-mediated cytotoxicity in a concentration-dependent manner. Incubation with ACE resulted in a significant reduction in IL-1beta and IFN-gamma-induced NO production, a finding that correlated well with reduced levels of the iNOS mRNA and protein. The molecular mechanism by which ACE inhibited iNOS gene expression appeared to involve the inhibition of NF-kappaB activation. The IL-1beta and IFN-gamma-stimulated RIN cells showed increases in NF-kappaB binding activity and p65 subunit levels in the nucleus, and IkappaBalpha degradation in cytosol compared to unstimulated cells. Furthermore, ACE restored the cytokine-induced inhibition of insulin release from isolated islets. These results suggest that ACE protects beta-cells by suppressing NF-kappaB activation.

Diabetes mellitus is characterized by cytokine-induced insulitis and a deficit in beta-cell mass. Ligands for peroxisome proliferator-activated receptor-gamma (PPAR-gamma) have been shown to have anti-inflammatory effects in various experimental models. We questioned whether activation of endogenous PPAR-gamma by either PPAR-gamma ligands or adenoviral-directed overexpression of PPAR-gamma (Ad-PPAR-gamma) could inhibit cytokine-induced beta-cell death in RINm5F (RIN) cells, a rat insulinoma cell line. Treatment of RIN cells with interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) induced beta-cell damage through NF kappaB-dependent signaling pathways. Activation of PPAR-gamma by PPAR-gamma ligands or Ad-PPAR-gamma inhibited IL-1 beta and IFN-gamma-stimulated nuclear translocation of the p65 subunit and DNA binding activity. NF kappaB target gene expression and their product formation, namely inducible nitric oxide synthase and cyclooxygenase-2 were decreased by PPAR-gamma activation, as established by real-time PCR, Western blots and measurements of NO and PGE(2). The mechanism by which PPAR-gamma activation inhibited NF kappaB-dependent cell death signals appeared to involve the inhibition of I kappa B alpha degradation, evidenced by inhibition of cytokine-induced NF kappaB-dependent signaling events by Ad-I kappaB alpha (S32A, S36A), non-degradable I kappaB alpha mutant. I kappaB beta mutant, Ad-I kappaB beta (S19A, S23A) was not effective in preventing cytokine toxicity. Furthermore, a protective effect of PPAR-gamma ligands was proved by assaying for normal insulin secreting capacity in response to glucose in isolated rat pancreatic islets. The beta-cell protective function of PPAR-gamma ligands might serve to counteract cytokine-induced beta-cell destruction.