Ultrathin-film growth of para-sexiphenyl (II): Formation of large-size domain and continuous thin film

The large-size domain and continuous para-sexiphenyl (p-6P) ultrathin film was fabricated successfully on silicon dioxide (SiO2) substrate and investigated by atomic force microscopy and selected area electron diffraction. At the optimal substrate temperature of 180 degrees C, the first-layer film exhibits the mode of layer growth, and the domain size approaches 100 mu m(2). Its saturated island density (0.018 mu m(-2)) is much smaller than that of the second-layer film (0.088 mu m(-2)), which begins to show the Volmer-Weber growth mode.

Highly efficient electrochemiluminescence of functionalized tris(2,2 '-bipyridyl)ruthenium(II) enrichment of its co-reactants

An enhanced electrochemiluminescence (ECL) efficiency is obtained from the ruthenium complex tris(2,2'-bipyridyl)ruthenium(II) (Ru(bpy)(3)(2+)) by introduction of an ionic liquid (IL) 1-butyl-3-methylimidazolium tetrafluoroborate (BMImBF(4)). Upon addition of 1% (v/v) BMImBF(4) to 0.1 mm Ru(bpy)(3)(2+) solution, a maximum increase in ECL intensity is obtained both at an indium tin oxide (ITO) electrode (15-fold) and at a glassy carbon (GC) electrode (5- to 64old). Furthermore, upon addition of 1% (v/v) BMImBF4 to 5 pm Ru(bpy)(3)(2+)/100 mm co-reactant systems at a GC electrode, IL adsorption occurs at the electrode surface, which results in a change of the polarity of the electrode surface. Such functionalization greatly improves the functions of both Ru(bpy)(3)(2+) and ionic liquids, as is demonstrated in the sensitive and selective concentration enrichment of the Ru(bpy)(3)(2+) co-reactants.

Catalysis of hydrotalcite-like compounds in liquid phase oxidation: (II) - Oxidation of p-cresol to p-hydroxybenzaldehyde

Hydrotalcite-like compounds (HTLcs): CoMAlCO3-HTLcs (M=Cu2+, Ni2+, Mn2+, Cr3+, Fe3+), were synthesized by coprecipitation and characterized with XRD and IR. The catalysis of these HTLcs and their calcined products were studied in the p-cresol oxidation, and the effects of the temperature of HTLcs calcination, the ratio of Co/Cu, different promoters, reaction temperatures and reaction times on reaction activities were investigated. It has been found that calcined HTLcs have higher activity than uncalcined samples and mechanical mixed oxides in this reaction. The best yield was obtained from the CoCuAlCO3-HTLc (Co/Cu/Al=3:1:1) calcined at 450 degrees C. A tentative reaction mechanism was also proposed. (C) 1998 Elsevier Science B.V.

Comparison of the NMR enantiodifferentiation of a chiral ruthenium(II) complex of C2 symmetry using the TRISPHAT anion and a lanthanide shift reagent

The tris[tetrachlorobenzenediolato]phosphate(v) anion (TRISPHAT) is known to be an efficient NMR chiral shift agent for various chiral cationic species. Here we compare the efficiency of TRISPHAT and of a chiral lanthanide shift reagent for the determination of the enantiomeric purity of the chiral building block [Ru(phen)[2]PY[2]][2][+] which possesses C[2] symmetry. We also discuss our results in terms of the geometry of interaction between the Ru(II) complex and the TRISPHAT anion.

A randomised phase II study of two different schedules of pegylated liposomal doxorubicin in metastatic breast cancer (EORTC-10993).

One hundred and sixteen women with measurable metastatic breast cancer participated in a randomised phase II study of single agent liposomal pegylated doxorubicin (Caelyx) given either as a 60 mg/m2 every 6 weeks (ARM A) or 50 mg/m2 every 4 weeks (ARM B) schedule. Patients were over 65 years of age or, if younger, had refused or been unsuitable for standard anthracyclines. The aims of the study were to evaluate toxicity and dose delivery with the two schedules and obtain further information on the response rate of liposomal pegylated doxorubicin as a single agent in anthracycline nai ve advanced breast cancer. Twenty-six patients had received prior adjuvant chemotherapy (including an anthracycline in 10). Sixteen had received non-anthracycline-based first-line chemotherapy for advanced disease. One hundred and eleven patients were evaluable for toxicity and 106 for response. The delivered dose intensity (DI) was 9.8 mg/m2 (95% CI, 7.2-10.4) with 37 (69%) achieving a DI of >90% on ARM A and 11.9 mg/m2 (95% CI, 7.5-12.8) with 37 (65%) achieving a DI of >90% on ARM B. The adverse event profiles of the two schedules were distinctly different. Mucositis was more common with the every 6 weeks regimen (35% CTC grade 3/4 in ARM A, 14% in ARM B) but palmar plantar erythrodysesthesia (PPE) was more frequent with the every 4 weeks regimen (2% CTC grade 3/4 in ARM A, 16% in ARM B). Confirmed objective partial responses by RECIST criteria were seen with both schedules; 15/51 (29%) on ARM A and 17/56 (31%) on ARM B. Liposomal pegylated doxorubicin showed significant activity in advanced breast cancer with a generally favourable side-effect profile. The high frequency of stomatitis seen with 6 weekly treatment makes this the less preferred of the two schedules tested.

Independent beta-arrestin 2 and G protein-mediated pathways for angiotensin II activation of extracellular signal-regulated kinases 1 and 2.

Stimulation of a mutant angiotensin type 1A receptor (DRY/AAY) with angiotensin II (Ang II) or of a wild-type receptor with an Ang II analog ([sarcosine1,Ile4,Ile8]Ang II) fails to activate classical heterotrimeric G protein signaling but does lead to recruitment of beta-arrestin 2-GFP and activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) (maximum stimulation approximately 50% of wild type). This G protein-independent activation of mitogen-activated protein kinase is abolished by depletion of cellular beta-arrestin 2 but is unaffected by the PKC inhibitor Ro-31-8425. In parallel, stimulation of the wild-type angiotensin type 1A receptor with Ang II robustly stimulates ERK1/2 activation with approximately 60% of the response blocked by the PKC inhibitor (G protein dependent) and the rest of the response blocked by depletion of cellular beta-arrestin 2 by small interfering RNA (beta-arrestin dependent). These findings imply the existence of independent G protein- and beta-arrestin 2-mediated pathways leading to ERK1/2 activation and the existence of distinct "active" conformations of a seven-membrane-spanning receptor coupled to each.

What the brain stem tells the frontal cortex. II. Role of the SC-MD-FEF pathway in corollary discharge.

One way we keep track of our movements is by monitoring corollary discharges or internal copies of movement commands. This study tested a hypothesis that the pathway from superior colliculus (SC) to mediodorsal thalamus (MD) to frontal eye field (FEF) carries a corollary discharge about saccades made into the contralateral visual field. We inactivated the MD relay node with muscimol in monkeys and measured corollary discharge deficits using a double-step task: two sequential saccades were made to the locations of briefly flashed targets. To make second saccades correctly, monkeys had to internally monitor their first saccades; therefore deficits in the corollary discharge representation of first saccades should disrupt second saccades. We found, first, that monkeys seemed to misjudge the amplitudes of their first saccades; this was revealed by systematic shifts in second saccade end points. Thus corollary discharge accuracy was impaired. Second, monkeys were less able to detect trial-by-trial variations in their first saccades; this was revealed by reduced compensatory changes in second saccade angles. Thus corollary discharge precision also was impaired. Both deficits occurred only when first saccades went into the contralateral visual field. Single-saccade generation was unaffected. Additional deficits occurred in reaction time and overall performance, but these were bilateral. We conclude that the SC-MD-FEF pathway conveys a corollary discharge used for coordinating sequential saccades and possibly for stabilizing vision across saccades. This pathway is the first elucidated in what may be a multilevel chain of corollary discharge circuits extending from the extraocular motoneurons up into cerebral cortex.