155 research outputs found

    Agus Aris Munandar, Ibukota Majapahit; Masa Jaya dan Pencapaian. Depok: Komunitas Bambu, 2008, X + 161 Pp. ISBN 979-37-31-39-7. Price: IDR 34,000 (Soft Cover).

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    Palladium-catalyzed cross-coupling reactions between chlorinated 1,3,5-triazines (TZ) and tetrathiafulvalene (TTF) trimethyltin derivatives afford mono- and <i>C</i><sub>3</sub> symmetric trisĀ­(TTF)-triazines as donorā€“acceptor compounds in which the intramolecular charge transfer (ICT) is modulated by the substitution scheme on TTF and TZ and by chemical or electrochemical oxidation. The TTF-TZ-Cl<sub>2</sub> and (SMe)<sub>2</sub>TTF-TZ-Cl<sub>2</sub> derivatives show fully planar structures in the solid state as a consequence of the conjugation between the two units. Electrochemical and photophysical investigations, supported by theoretical calculations, clearly demonstrate that the lowest excited state can be ascribed to the intramolecular charge transfer (ICT) Ļ€Ā­(TTF)ā†’Ļ€*Ā­(TZ) transition. The trisĀ­(TTF) compound [(SMe)<sub>2</sub>TTF]<sub>3</sub>-TZ shows fluorescence when excited in the ICT band, and the emission is quenched upon oxidation. The radical cations TTF<sup>+ā€¢</sup> are easily observed in all of the cases through chemical and electrochemical oxidation by steady-state absorption experiments. In the case of [(SMe)<sub>2</sub>TTF]<sub>3</sub>-TZ, a low energy band at 5000 cm<sup>ā€“1</sup>, corresponding to a coupling between TTF<sup>+ā€¢</sup> and TTF units, is observed. A crystalline radical cation salt with the TTF-TZ-Cl<sub>2</sub> donor and PF<sub>6</sub><sup>ā€“</sup> anion, prepared by electrocrystallization, is described

    Electrophoresis of representative PCR products of HPV on 2.0% agarose gel.

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    <p>M: Marker (TaKaRa DL2000); Lane1-5: nested PCR products; Lane 6ā€“11: type-specific PCR products; Lane 1, 6 and 9 are positive controls; Lane 5, 8 and 11 show negative controls. Lanes 2ā€“4 show positive bands of 140 bp, Lane 7 and 10 show positive bands of 315 bp and 152 bp, respectively.</p

    Clinical and pathological features of paraffin-embedded samples of breast cancer (BC) and breast benign disease (BBD).

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    <p>Clinical and pathological features of paraffin-embedded samples of breast cancer (BC) and breast benign disease (BBD).</p

    A New Insight into Catalytic Ozonation with Nanosized Ceā€“Ti Oxides for NO<sub><i>x</i></sub> Removal: Confirmation of Ceā€“Oā€“Ti for Active Sites

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    Amorphous cerium and titanium mixed oxides (Am-CeTi) and crystalline cerium and titanium mixed oxides (Ct-CeTi), prepared by coprecipitation and impregnation methods, respectively, were successfully utilized in catalytic ozonation for NO<sub><i>x</i></sub> removal. The catalytic activity has been confirmed to be determined by the concentration of Ā·OH radicals. Am-CeTi shows higher activity than Ct-CeTi. Ceā€“Oā€“Ti linkage bonds, with an interaction between Ce and Ti on an atomic scale, are confirmed for the first time to be an active site for catalytic ozonation to remove NO<sub><i>x</i></sub>. The incorporation of more Ce results in an amorphous structure (Am-CeTi) and a higher number of Ceā€“Oā€“Ti linkage bonds as compared to that of Ct-CeTi, and the Ceā€“Oā€“Ti structure is directly observed by HR-TEM. Moreover, such incorporation is responsible for less surface defects and lower densities of surface hydroxyl groups because of the elimination of crystalline defects. The higher catalytic activity of Am-CeTi indicates the small effect of surface defects and surface groups

    Improvement in the Etching Performance of the Acrylonitrileā€“Butadieneā€“Styrene Resin by MnO<sub>2</sub>ā€“H<sub>3</sub>PO<sub>4</sub>ā€“H<sub>2</sub>SO<sub>4</sub> Colloid

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    The present study aimed to evaluate the surface etching of the acrylonitrileā€“butadieneā€“styrene (ABS) resin in the MnO<sub>2</sub>ā€“H<sub>3</sub>PO<sub>4</sub>ā€“H<sub>2</sub>SO<sub>4</sub> colloid. To enhance the soluble MnĀ­(IV) ion concentration and improve the etching performance of ABS resin, H<sub>3</sub>PO<sub>4</sub> was added as a complexing agent into the MnO<sub>2</sub>ā€“H<sub>2</sub>SO<sub>4</sub> etching system. The effects of the H<sub>2</sub>SO<sub>4</sub> concentration and etching time on the surface topography, surface roughness, adhesion strength, and the surface chemistry of the ABS substrates were investigated. The optimal oxidation potentials of MnO<sub>2</sub> in the colloids decreased from 1.426 to 1.369 V with the addition of H<sub>3</sub>PO<sub>4</sub>. Though the etching conditions changed from 70 Ā°C for 20 min to 60 Ā°C for 10 min, the adhesion strength between the ABS substrates and electroless copper film increased from 1.19 to 1.33 KN/m after etching treatment. This could be attributed to the significant increase of the soluble MnĀ­(IV) ion concentration in the MnO<sub>2</sub>ā€“H<sub>3</sub>PO<sub>4</sub>ā€“H<sub>2</sub>SO<sub>4</sub> colloid. The surface chemistry results demonstrated that the oxidation reaction of āˆ’Cī—»Cā€“ bonds in the polybutadiene phase was accelerated in the etching process by the addition of H<sub>3</sub>PO<sub>4</sub>, and the abundant āˆ’COOH and āˆ’OH groups were formed rapidly on the ABS surface with the etching treatment. These results were in agreement with the results of surface scanning electron microscopic observations and adhesion strength measurement. The results suggested that the MnO<sub>2</sub>ā€“H<sub>3</sub>PO<sub>4</sub>ā€“H<sub>2</sub>SO<sub>4</sub> colloid was an effective surface etching system for the ABS surface roughness

    MicroRNA 181b Regulates Decorin Production by Dermal Fibroblasts and May Be a Potential Therapy for Hypertrophic Scar

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    <div><p>Hypertrophic scarring is a frequent fibroproliferative complication following deep dermal burns leading to impaired function and lifelong disfigurement. Decorin reduces fibrosis and induces regeneration in many tissues, and is significantly downregulated in hypertrophic scar and normal deep dermal fibroblasts. It was hypothesized that microRNAs in these fibroblasts downregulate decorin and blocking them would increase decorin and may prevent hypertrophic scarring. Lower decorin levels were found in hypertrophic scar as compared to normal skin, and in deep as compared to superficial dermis. A decorin 3ā€™ un-translated region reporter assay demonstrated microRNA decreased decorin in deep dermal fibroblasts, and microRNA screening predicted miR- 24, 181b, 421, 526b, or 543 as candidates. After finding increased levels of mir-181b in deep dermal fibroblasts, it was demonstrated that TGF-Ī²<sub>1</sub> stimulation decreased miR-24 but increased miR-181b and that hypertrophic scar and deep dermis contained increased levels of miR-181b. By blocking miR-181b with an antagomiR, it was possible to increase decorin protein expression in dermal fibroblasts. This suggests miR-181b is involved in the differential expression of decorin in skin and wound healing. Furthermore, blocking miR-181b reversed TGF-Ī²<sub>1</sub> induced decorin downregulation and myofibroblast differentiation in hypertrophic scar fibroblasts, suggesting a potential therapy for hypertrophic scar.</p></div

    Relative expression of miR-181b in matched superficial and deep dermis and site-matched NS and HSc biopsies.

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    <p>Total RNA was extracted from tissue specimens using a chilled pestle and mortar and Trizol for relative quantitation using RT-qPCR. (a) Relative expression of miR-181b in matched superficial and deep dermis of NS (mean Ā± SEM, n = 3 samples per patient, * P < 0.001). (b) Relative expression of miR-181b in matched NS and HSc (mean Ā± SEM, n = 3 samples per patient, * P < 0.05, ** P < 0.01).</p

    Evidence for the involvement of miRNA in <i>DCN</i> downregulation in DF.

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    <p>Total RNA was extracted from SF and DF cell culture after 48 hours and relative expression of selected miRNA quantitated using RT-qPCR (mean Ā± SEM, n = 3, * P < 0.05).</p

    Regulation of DCN by miR-181b.

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    <p>HEK293A were cultured in DMEM + 2% FBS and transfected with pmirGLO constructs containing various miRNA binding sites and (a) relative fluorescence quantitated using a luminometer to determine relative knockdown by miR-181b (mean Ā± SEM, n = 4, *** P ā‰¤ 0.01). SF were cultured in DMEM + 2% FBS and transfected with miR-control, synthetic miR-181b or siRNA-DCN and (b) DCN protein in supernatant was measured by ELISA (mean Ā± SEM, n = 3, ** P < 0.03), and (c) DCN mRNA was measured using RT-qPCR on total RNA (mean Ā± SEM, n = 3, * P < 0.05). (d) DF were cultured in DMEM + 2% FBS and transfected with antagomiR-control (amiR-control) or antagomiR-181b (amiR-181b) and DCN protein in supernatant was measured by ELISA (mean Ā± SEM, n = 3, *** P < 0.01).</p

    Regulation of miRNA expression by TGF-Ī²<sub>1</sub> in SF and DF.

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    <p>Cells were cultured in DMEM + 2% FBS with the indicated treatment protocols and total RNA extracted for RT-qPCR. (a) Dose-response curve showing relative expression of miR-24 for SF and DF cultured in increasing concentrations of TGF-Ī²<sub>1</sub> for 48 hours (mean Ā± SEM, n = 3). (b) Dose-response curve showing relative expression of miR-181b for SF and DF culutured in increasing concentrations of TGF-Ī²<sub>1</sub> for 48 hours (mean Ā± SEM, n = 3, * P < 0.05, ** P < 0.01). (c) Time-response curve showing relative expression of miR-181b for SF and DF at fixed concentrations of TGF-Ī²<sub>1</sub> (SF 10 ng/mL, DF 20 ng/mL) (mean Ā± SEM, n = 3, * P < 0.03).</p
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