Efficiency enhancement of dye-sensitized solar cells by the addition of an oxidizing agent to the TiO(2) paste.

The addition of various amounts of a strong oxidizing agent (3,5-dinitrosalicyclic acid, DNSA) to TiO2 paste enhances the solar-to-electrical-energy conversion efficiency of the corresponding dye-sensitized solar cells (DSSCs). Maximum performance was obtained from a device that was fabricated by using a TiO2 paste with 2 wt % DNSA, which showed a short-circuit current density of 17.88 mA cm(-2) , an open-circuit voltage of 0.78 V, and an overall conversion efficiency of 9.62 %, which was an improvement in comparison to reference cells without DNSA. This improvement was rationalized in terms of the amount of residual carbon (formed due to the oxidation of binders) remaining on the TiO2 surface. Addition of a larger amount of oxidizing agent led to a smaller amount of residual carbon on the TiO2 surface. This smaller amount of residual carbon enhanced the adsorption of a larger number of dye molecules on the TiO2 surface. The addition of an oxidizing agent facilitated the removal of more residual organic species during the high-temperature calcination process while causing no change in the surface morphology and microstructure of the TiO2 film.

Prediction of rock salt structure of (InN)32 nanoparticles from first principles calculations.

From first principles calculations, we show that (InN)32 nanoparticles favor rock salt structure compared with wurtzite structure in bulk. A phase transition from wurtzite to rock salt structure is known to occur in bulk InN at 12.1 GPa and higher values of pressure for AlN and GaN. However, at the nanoscale we show that this structural transition takes place in (InN)32 without applying pressure. The charge asymmetry value "g" and cation/anion size ratio in InN describe very well this behavior. Similar studies on nanoparticles of AlN and GaN as well as a few other binary compounds such as MgS, AgI, ZnO, and CdSe, however, do not show such a transition. Our results suggest (InN)32 to be a unique candidate as further calculations on a few larger size (InN)n nanoparticles show that a filled cage (two shells) (InN)12@(InN)48 structure of (InN)60 has higher binding energy compared with a rock salt structure of (InN)64 leading to the conclusion that other 3D structures are likely to become favorable over rock salt structure for larger sizes.

Interactions between multiwall carbon nanotubes and poly(diallyl dimethylammonium) chloride: effect of the presence of a surfactant.

The interactions between multiwall carbon nanotubes (MWCNTs) and poly(diallyl dimethylammonium) chloride (PDDA) have been studied in the presence of different ionic and nonionic surfactants, such as sodium dodecyl sulfate (SDS), cetyltrimethylammonium bromide (CTAB), Tween 20, 40, 60, and 80, and Triton X-100. On the basis of scanning electron microscopy (SEM) results, the MWCNT/PDDA sample treated with Triton X-100 has been observed to show good dispersion of nanotubes. This is due to the π-π stacking between the benzene ring of Triton X-100 and the hexagonal carbon rings of nanotubes and better coating of PDDA on MWCNTs, as is confirmed by the Raman studies. Energy dispersive X-ray (EDX) spectroscopic data shows the presence of higher oxygen content in the MWCNTs/PDDA/Triton X-100 sample. The maximum upshift in the C1s peak position and down-shift in the N1s peak position for the MWCNTs/PDDA/Triton X-100 sample has been observed from X-ray photoelectron spectroscopy (XPS) results and is due to the intermolecular charge transfer from carbon in MWCNTs to nitrogen in PDDA. The presence and nature of a surfactant in the MWCNTs/PDDA system has been found to affect their interactions. The above results suggest that the MWCNTs/PDDA/Triton X-100 system is suitable as a metal-free electrocatalyst for the oxygen reduction reaction (ORR) in fuel cells.

Study of ion diffusional motion in ionic liquid-based polymer electrolytes by simultaneous solid state NMR and DTA.

Polymer electrolytes containing ionic liquid (IL), 2-methyl-1,3-dipropylimidazolium dihydrogenphosphate (MDPImH2PO4) have been studied by (1)H solid state NMR and differential thermal analysis (DTA) simultaneously by using a specially designed probe. To the best of our knowledge, this is the first report of its kind for IL based polymer electrolytes. The variation of NMR line width with temperature for the IL and polymer electrolytes shows line narrowing at the glass transition and melting temperature. The onset of long-range ion diffusional motion also takes place at these temperatures and is accompanied by a sudden increase in ionic conductivity value by 2-3 orders of magnitude. The presence of amorphous and crystalline phases in IL-based polymer electrolytes has been observed from X-ray diffraction (XRD) studies, and the amorphous phase is the high conducting phase in these polymer electrolytes. The IL-based polymer electrolytes have been observed to be thermally stable up to 200 °C. The results obtained from ion transport studies have also been supported by Fourier transform infrared (FTIR), XRD, and cyclic voltammetry (CV) studies.

Correlation between ion diffusional motion and ionic conductivity for different electrolytes based on ionic liquid.

Room temperature ionic liquid 2,3-dimethyl-1-hexylimidazolium bis(trifluoromethane sulfonyl)imide (DMHxImTFSI) has been synthesized and used in the preparation of polymer gel electrolytes containing polymethylmethacrylate and propylene carbonate (PC). The onset of ion diffusional motion has been studied by (1)H and (19)F NMR spectroscopy and the results obtained for ionic liquid, liquid electrolytes, and polymer gel electrolytes have been correlated with the ionic conductivity results for these electrolytes in the 100-400 K temperature range. The temperature at which (1)H and (19)F NMR lines show motional narrowing and hence ion diffusional motion starts has been found to be closely related to the temperature at which a large increase in ionic conductivity has been observed for these electrolytes. Polymer gel electrolytes have high ionic conductivity over a wide range of temperatures. Thermogravimetric analysis/differential scanning calorimetry studies show that the ionic liquid (DMHxImTFSI) used in the present study is thermally stable up to 400 degrees C, whereas the addition of PC lowers the thermal stability of polymer gel electrolytes containing the ionic liquid. Different electrolytes have been observed to show high ionic conductivity in different range of temperatures, which can be helpful in the design of polymer gel electrolytes for specific applications.

Comparison of prostaglandin and cimetidine in protection of isolated gastric glands against indomethacin injury.

Prostaglandins can protect the in vivo gastric mucosa against necrosis produced by a variety noxious agents. Cimetidine has also been shown to have protective properties in humans and in some models of experimental injury. Whether prostaglandins or cimetidine may protect gastric mucosal cells directly in the absence of systemic factors remains controversial. In the present study, the potential protective actions of prostaglandin and cimetidine against indomethacin injury were assessed in isolated rat gastric glands. Gastric glands were pre-incubated in oxygenated medium with either placebo, 16,16 dimethyl prostaglandin E(2) (dm PGE(2)) or cimetidine and incubated at 37 degrees C in medium containing 0.5 mg/ml of indomethacin for 2, 4 and 6 hrs. Cell injury and protection was assessed by the Fast Green exclusion test (viability test), leakage of lactate dehydrogenase (LDH) into the medium, and by scanning and transmission electron microscopy. In addition, the generation of PGE(2) by the gland cells was determined using RIA assay. Indomethacin by itself significantly reduced the viability of gastric glands, increased LDH release into the medium and produced prominent ultrastructural damage. In contrast to cimetidine, co-incubation of gastric glands with dm PGE(2) added to indomethacin, significantly reduced indomethacin-induced injury, increased the number of viable cells, reduced LDH leakage and diminished the extent of ultrastructural damage. The dose of indomethacin (5 microg/ml) which significantly inhibited the generation of PGE(2) (up to 90% inhibition) had no effect on cell viability nor LDH release. We conclude that 1) exogenous PGE2 exerts a potent protective activity in vitro which is independent on neural, vascular and hormonal factors; 2) inhibition of endogenous PGs may not the primary mechanism in the deleterious action of indomethacin against damage to gastric glandular cells and 3) indomethacin can exert a direct cytotoxic effect on the mucosal cells in gastric glands.

Polymer electrolytes based on room temperature ionic liquid: 2,3-dimethyl-1-octylimidazolium triflate.

Room temperature ionic liquid (DMOImTf) based upon 2,3-dimethyl-1-octylimidazolium cation and trifluoromethanesulfonate or triflate (CF(3)SO(3))(-) anion has been synthesized and shows conductivity of 5.68 mS/cm and viscosity of 26.4 cP at 25 degrees C. Ion conducting polymer electrolytes based on polymers (poly(ethylene oxide) (PEO) and polyvinylidenefluoride-co-hexafluoropropylene (PVdF-HFP)) and ionic liquid (DMOImTf) were prepared in film form by the casting technique. The conductivity of polymer electrolytes containing 0.5 M LiCF(3)SO(3) in PEO:DMOImTf taken in equal weight ratio increases with the addition of propylene carbonate (PC) while its mechanical stability improved by dispersing nanosize fumed silica. However, polymer electrolytes containing PVdF-HFP and ionic liquid show a high value of conductivity (10(-4)-10(-3) S/cm) alongwith better mechanical stability.

Isolation of morphologically and functionally intact gastric mucosal microvessels rapid communication.

Gastric mucosal microvessels were isolated after arterial perfusion of the rat stomach with magnetized iron oxide suspension. After homogenization of scrapped gastric mucosa, microvessels were initially separated with a high power magnet and further separated and purified by using a nylon sieve. Aliquots of purified microvessels were assessed for viability, histologic appearance, ultrastructure and generation of prostacyclin. Microvessels were plated on Matrigel and cultured in DMEM with high glucose and 10% FBS for 1, 3 or 5 days. After 1, 3 and 5 days of culturing, endothelial viability was assessed with Fast green exclusion, and the basal and stimulated (with calcium ionophore) generation of prostacyclin was determined by assaying aliquots of the incubating medium for 6-keto PGF(1alpha). At 1 and 3 hrs after isolation, microvessels demonstrated intact morphologic structures as reflected by transmission EM and 92+/-4% of viable endothelial cells. The microvessels plated on Matrigel maintained good viability for at least 5 days and generated prostacyclin at the baseline and following ionophore stimulation. These data demonstrate that isolated microvessels cultured under optimal conditions are fully viable and functional.

Macrophages can recognize and kill tumor cells bearing the membrane isoform of macrophage colony-stimulating factor.

NBXFO hybridoma cells produced both the membrane and secreted isoforms of macrophage colony-stimulating factor (M-CSF). Murine bone marrow cells stimulated by the secreted form of M-CSF (sM-CSF) became Mac1+, Mac2+, Mac3+, and F4/80+ macrophages that inhibited the growth of NBXFO cells, but not L1210 or P815 tumor cells. In cytotoxicity studies, M-CSF activated macrophages and freshly isolated macrophages killed NBXFO cells in the presence of polymyxin B, eliminating the possibility that contaminating lipopolysaccharide (LPS) was responsible for the delivery of the cytotoxic signal. Retroviral-mediated transfection of T9 glioma cells with the gene for the membrane isoform of M-CSF (mM-CSF), but not for the secreted isoform of M-CSF, transferred the ability of macrophages to kill these transfected T9 cells in a mM-CSF dose-dependent manner. Macrophage-mediated killing of the mM-CSF transfected clone was blocked by using a 100-fold excess of recombinant M-CSF. Catalase, superoxide dismutase, and the nitric oxide inhibitor, N-omega-nitro-arginine methyl ester (NAME), did not effect macrophage cytotoxicity against the mM-CSF transfectant T9 clones. T9 parental cells when cultured in the presence of an equal number of the mM-CSF transfectant cells were not killed, indicating specific target cell cytotoxicity by the macrophages. Electron microscopy showed that macrophages were capable of phagocytosizing mM-CSF bearing T9 tumor cells and NBXFO hybridoma cells; this suggested a possible mechanism of this cytotoxicity. This study indicates that mM-CSF provides the necessary binding and triggering molecules through which macrophages can initiate direct tumor cell cytotoxicity.

Macrophage colony stimulatory factor-activated bone marrow macrophages suppress lymphocytic responses through phagocytosis: a tentative in vitro model of Rosai-Dorfman disease.

NBXFO hybridoma cells produced macrophage colony-stimulating factor (M-CSF), which stimulated the growth of murine bone marrow-derived macrophages with potent suppressor activity. These macrophages suppressed lymphocyte responses to mitogens and antigens in a dose-dependent manner. Using a transwell chamber, we demonstrated that macrophages needed physical contact with the lymphocytes to suppress lymphocyte proliferation on day 1 in the concanavalin A mitogen reaction. In addition, no soluble suppressor factor was detected at that time. The number of lymphocytes disappeared with time when they were cocultured with the macrophages. Electron microscopy revealed that the macrophage phagocytosized the lymphocytes after 7 1/2 h. Dextran sulfate, heparan, and fucoidan prevented the macrophages from suppressing the lymphocytes. This phenomenon resembles the human disease sinus histiocytosis, also called Rosai-Dorfman disease, in which macrophages (histiocytes) phagocytosize autologous lymphocytes; occasionally, this disease is associated with immunological abnormalities. Thus we believed that macrophage-activating cytokines, such as M-CSF, may stimulate macrophages to phagocytose lymphocytes in vivo.

Salicylate effects on a monolayer culture of gastric mucous cells from adult rats.

Aspirin, acetyl salicylic acid, damages gastric mucosal cells. This effect is considered related to its inhibition of prostaglandin synthesis. On the other hand, sodium salicylate has been reported to be cytoprotective against drug damage to gastric mucosa in vivo. One reason for this difference is that salicylic acid, unlike acetyl salicylic acid does not inhibit prostaglandin synthesis by gastric mucosa in vivo. Previous studies on tissue culture cells from our laboratory have required gastric mucosa from fetal rats; this was time consuming and expensive. The purpose of this study was to develop a primary cell culture of adult rat fundic epithelial cells and to test the effect of sodium salicylate on: (1) prostaglandin (PGE2) production, (2) cell viability, (3) reducing cell damage by sodium taurocholate. Gastric epithelial cells were isolated from adult rat stomachs and cultured on collagen gel. Cells reached confluency on day 4 at which stage fibroblasts were rarely seen (less than 1%). Autoradiographic study showed that cultured cells incorporated [3-H] thymidine into nuclei. In histochemical studies, 94% of the cells contained PAS positive granules (mucous cells). Mucous granules were observed in the cytoplasm of the majority of cells by electronmicroscopy. These cells synthesised prostaglandin E2 as determined by radioimmunoassay. Indomethacin 10(-4) M strongly suppressed PGE2 production after 30 minutes while 10(-3) and 10(-4)M sodium salicylate had no effect. Pharmacologic concentrations of 10 mM sodium salicylate had no effect on PGE2 production at 30 minutes and only weakly inhibited production after one hour incubation. Sodium salicylate up to 30 mM had no effect on cell viability, a concentration of 50 mM being necessary to produce significant cell damage. Sodium salicylate 10 mM significantly protected cells against damage induced by 10 mM sodium taurocholate. We conclude: (i) adult rat gastric mucous epithelial cells can be successfully cultured in vitro; (ii) prostaglandin synthesis is inhibited by indomethacin but not by low doses of sodium salicylate; (iii) sodium salicylate does not damage gastric mucosal cells except at very high concentrations; (iv) sodium salicylate protects against damage to cells induced by sodium taurocholate.

Cytoprotective effect of acetaminophen against taurocholate-induced damage to rat gastric monolayer cultures.

Acetaminophen has recently been reported to protect against drug damage to gastric mucosa in vivo. The present study tested acetaminophen protection in cultured rat gastric mucous cells against sodium taurocholate-induced damage and assessed the role of endogenous prostaglandins. Cell damage was assessed by phase-contrast microscopy and quantitated by Chromium-51 release assay which positively correlated with the trypan blue dye exclusion test (r = 0.98). The effect of acetaminophen on the production of PGE2 and 6-keto-prostaglandin F1a (6KF) was also studied. Sodium taurocholate caused cell death in a dose-dependent manner as indicated by increased 51Cr release. Preincubation with 5 mM acetaminophen significantly reduced 51Cr release caused by 5 mM sodium taurocholate, producing a 40% increase in cell survival. This cytoprotection was not blocked by indomethacin. PGE2 and 6KF of the media did not change after preincubation with nondamaging concentrations of acetaminophen or taurocholate. These results indicate that: (1) acetaminophen exerts a direct protective effect on gastric mucous cells cultured in vitro independent of indirect factors such as blood flow and (2) this protection is not associated with increased prostaglandin production.

Human cell line for study of damage to gastric epithelial cells in vitro.

UNLABELLED: We evaluated whether monolayers from a well-differentiated human gastric epithelial cell line (MKN 28) are suitable for studying the effect of drugs on gastric mucosa. MKN 28 monolayers and monolayers of human gastric epithelial cells from surgical specimens were studied morphologically and functionally. The protective effect of acetaminophen against taurocholate-induced damage was evaluated as was its effect on prostaglandin production. Both types of cultures showed similar morphologic and histochemical characteristics. Indomethacin inhibited and arachidonic acid stimulated prostaglandin production by both types of monolayers similarly. Both monolayers responded similarly to drug-induced damage. Acetaminophen decreased taurocholate-induced damage by 33% and 40% in MKN 28 cells and in primary human gastric cell culture, respectively. Indomethacin did not prevent acetaminophen protection nor did the amount of prostaglandin produced by cells increase after incubation with acetaminophen. IN CONCLUSION: (1) in the MKN 28 cell line model acetaminophen protected against taurocholate-induced damage; the percentage of protection was similar to that in primary cultures of human gastric epithelial cells; (2) acetaminophen protection in both models was not related to increased prostaglandin production; (3) the MKN 28 cell line is a suitable model to study damage to and protection of gastric epithelial cells in vitro.

Effects of excess dietary cholesterol on adrenal cholesterol accumulation and steroidogenesis.

Rats maintained on diets containing 3% cholesterol for 10 weeks show marked increase in adrenal cholesterol content. The greatest part of the increase is in the cholesterol ester fraction (329%), although free cholesterol is also elevated (140%). Morphologically, a marked increase in the lipid droplet content of the cells is observed. The microsomal fraction was enriched in cholesterol with parallel increases in microsomal ACAT activity in both normal and supplemented groups. Neutral cytosolic cholesterol esterase is unaffected by the diet. No significant increase in cholesterol occurred in the mitochondrial fraction. However, cholesterol binding to cytochrome P450 was affected by the diet under certain conditions. Cholesterol supplementation elevates adrenal corticosteroid levels (43%). Mild stress results in greater increases in adrenal corticosteroids after dietary supplementation. Aminoglutethimide produces inhibition of the stress induced increase in adrenal corticosteroids. This inhibition is less pronounced in cholesterol supplemented animals than in normal animals. The lack of similar effects on plasma corticosteroid levels suggests that enhanced metabolism and clearance of the plasma corticosteroids may be taking place.

A monolayer culture of human gastric epithelial cells.

Our aim was to develop a fibroblast-free monolayer culture of human gastric mucosal cells, using the specimens obtained by routine endoscopic biopsy. Human gastric mucosa obtained from normal volunteers by endoscopic biopsy was dissociated from collagenase and hyaluronidase. Dissociated cells were cultured in supplemented Coon's modified Ham's F-12 medium. Within 24 hr of inoculation, the cells were attached to the culture dishes. This was followed by cellular outgrowth. On phase-contrast microscopy, all cells had epithelial characteristics and fibroblasts were not observed. Ninety percent of cells contained periodic acid Schiff reaction-positive mucous granules after diastase digestion consistent with mucous epithelial cells. Two percent of the cells gave a strong reaction for succinic dehydrogenase activity (parietal cells). Immunohistochemical staining for pepsinogen in cultured cells was negative. On EM, microvilli-like projections, junctional complexes, Golgi apparatus, and mucous granules were apparent in the majority of cells. Mitotic figures were observed by day 3 with Giemsa staining. Autoradiographically, these cells were able to incorporate [3H]TdR into the nuclei. Cells were capable of synthesizing DNA, and this function was inhibited by cycloheximide. Cells could be cultured for up to two weeks without fibroblast contamination. A method of primary monolayer culture of human gastric mucosa obtained by a routine endoscopic biopsy has been successfully developed.

Cell culture of rat gastric fundic mucosa.

The purpose of this study was to develop a primary cell culture system of rat gastric fundic epithelial cells. The cells, isolated enzymatically, were cultured in Coon's modified Ham's F-12 medium supplemented with 10% fetal bovine serum, 15 mM HEPES buffer, fibronectin, and antibiotics. The inoculated cells started to grow rapidly on day 1 (doubling time, 26 h). The cells reached confluency on day 3. On phase contrast microscopy, over 90% of cells possessed epithelial characteristics. Histochemical studies showed (a) 90% of the epithelial cells contained PAS positive granules, (b) 5% of the cells gave a strong reaction for succinic dehydrogenase activity (presumably parietal cells), and (c) immunohistochemical localization of pepsinogen was negative. Ultrastructurally, microvilluslike structures, junctional complexes, Golgi apparatus, mitochondria, rough-surfaced endoplasmic reticulum, and mucous granules were observed. Mitotic figures were clearly observed on Giemsa staining and the mitotic index was maximum on day 2. Autoradiographic and biochemical studies showed these cells possessed the capability to synthesize deoxyribonucleic acid and this ability was maximum on day 2. These cells were able to synthesize and to secrete glycoprotein and this function was significantly increased by 16,16-dimethyl prostaglandin E2. Cyclic adenosine monophosphate produced by the cultured cells was enhanced by addition of 16,16-dimethyl prostaglandin E2 (p less than 0.01). This in vitro system provides a valuable model for studies of cellular functions of gastric mucosa.