Transparent anti-stain coatings with good thermal and mechanical properties based on polyimide-silica nanohybrids.

In this work, we synthesized polyimide/silica hybrid materials via sol-gel method using a fluorinated poly(amic acid) silane precursor and a variety of perfluorosilane contents. We studied the influence of a hybrid coating film with the following characteristics; hydrophobicity, oleophobicity, optical transparency, and surface hardness of the coating films. The hybrid coatings with the fluorosilane contents up to 10 wt% are optically transparent and present good thermal stability with a degradation temperature of > 500 degrees C as well as a glass transition of > 300 degrees C. Both water contact angle and oil contact angle increase rapidly with introducing small amount of the fluorosilane in the hybrids and reaches the maximum of 115 degrees and 61 degrees, respectively. The hardness of the hybrid coatings increases up to 5H with an increase of the FTES content in the hybrids. These colorless, transparent, and thermally stable hybrid materials could be suitable for applications as anti-stain coatings.

Activation of peroxisome proliferator-activated receptor-gamma protects pancreatic beta-cells from cytokine-induced cytotoxicity via NF kappaB pathway.

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.

Coptidis rhizoma extract protects against cytokine-induced death of pancreatic beta-cells through suppression of NF-kappaB activation.

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.

Induction of G1 arrest and apoptosis by Scutellaria barbata in the human promyelocytic leukemia HL-60 cell line.

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 G1 phase arrest of the cell cycle. This effect was associated with a marked decrease in the protein expression of cyclin A, D1, 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-G1 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.

Inhibitory effect of Artemisia capillaris extract on cytokine-induced nitric oxide formation and cytotoxicity of RINm5F cells.

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.

Induction of apoptosis by Radix Paeoniae Alba extract through cytochrome c release and the activations of caspase-9 and caspase-3 in HL-60 cells.

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.

Atomic Layer Deposition of Zirconium-Based High-k Metal Gate Oxide: Effect of Si Containing Zr Precursor.

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.

Factors Influencing Self-Identity and Menopausal Symptoms on Level of Depression in Middle Aged Women.

PURPOSE: The purpose of this study was to identify the factors influencing self-identity and menopausal symptoms their influence on level of depression in middle-aged woman. METHODS: Participants were 135 middle-aged women who were living in city B, were 45-60 years old, informed of study purpose, and agreed to participate. Data were collected from December, 2012 to January, 2013 using scales measuring depression, self-identity, and menopausal symptoms. Data were analyzed using t-test, ANOVA, Scheffe test, Pearson Correlation Coefficients, and Multiple Stepwise Regression. RESULTS: Level of depression was low, self-identity was slightly high, and menopausal symptoms were relatively low in these middle-aged women. There were significant differences in depression by perceived health status and perceived economic status. Depression had a moderate negative correlation with self-identity (r=-.49, p<.001) and a moderate positive correlation with menopausal symptoms (r=.57, p<.001). Menopausal psychological symptoms were the factor most affecting depression and explained 37% of the variance in depression. A total of 51% of variance in depression was explained by menopausal symptoms (psychological and physical), self-identity, and perceived economic status. CONCLUSION: Thus, an effort to improve self-identity, especially a plan to attenuate menopausal psychological symptoms is needed to reduce depression.

Flavonoids protect against cytokine-induced pancreatic beta-cell damage through suppression of nuclear factor kappaB activation.

OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.